And this has been one of, you know, an exciting year for cervical cancer science. We've seen a lot of exciting developments in this field, and it's been a long time coming, as you'll see during this presentation. You know, the IGCS is committed to providing meaningful opportunities to our industry colleagues to gain exposure to our gynecologic oncology community through unique year-long educational engagement programs. This platform provides the level of strategic engagement and exposure needed to educate and inform gynecologic oncology professionals on current and future educational opportunities and treatment management options, as well as to optimize patient care, both locally and globally. We're really passionate about that, as you know. And so, you know, not that you have to see my face again, but here I am here. And I'm really excited to be able to do this for you. So before we get started, I just want to mention a few housekeeping items. Please know that we're going to record this, and it will be on our IGCS Education 360 Learning Portal. If you guys have not been to this portal, you've got to go. It's phenomenal. It's so easy to use. It's user-friendly, and the content that's there is amazing. We'll continue to add to it all the time. I was able to beta test it, and I was just so excited to see the options that were available to it, the way it could be navigated so easily. So really excited to see this go live. Please, please, please check it out. It is an incredible benefit of the society, and I think you're going to really enjoy it. And as I always like to say, you know, don't be afraid to give us some feedback, because it's actually through this kind of interaction that we can enhance what we can deliver for your needs, educational needs. We think we have it all figured out, and we don't, obviously. So we're always open to your feedback. If you say, hey, listen, it would be great if we could do blank, send it to us, and we'll work on it and see if we can get it incorporated into the system. As you guys know how to do webinars, try to fit it to your window. Only the presenters will be able to speak, and the attendees' microphones are muted. So please use the chat function to get, or the question and answer session so we can get the questions into the queue, and we can take a look at it during the program and be able to address it at the end. These are my disclosures, and I'm happy to move on to the program here. So I know one of the beauties of IGCS is that we engage a global audience. And there's probably no more well-descripted cancer that affects the global population than cervical cancer. For those of you who are joining us all over the globe, you know, you can see where your country is and what that burden of disease is. We see it as the tremendous global healthcare crisis. I think that's the appropriate word here, because this is a disease which is completely preventable. And obviously, that's where our focus lies, that we can never have to talk about cancer development. We would love to talk about identification and prevention of cancer and pre-invasive disease so that we can be treated. Obviously, the burden of disease is not equitable with where the resources are, and that provides us an incredible need to expand our ability to reach the patients who need it most. Now, we've done, you know, this talk is focused on recurrent disease setting, and this has, as I mentioned in my opening comments, it has taken a lot of years to kind of get to see some of this rapid progress that we've seen in the last year. But it's important to kind of review the groundwork that was done before that. And so, what I've listed here on this slide is really a decades-plus work of the GOG. And of course, this is not to not recognize other investigators around the world who have contributed to this, to the science here. But just to highlight here that within the GOG, there was a series of trials that were done, mostly sequential, phase two trials to try to do an exploration for agents that might be active. And so, I've listed here on the right-hand side the Q, and the bottom there, you can see it's like 127, you know, with the alphabet. And this was really done to kind of sequentially monitor new drugs that kind of came in. And most of these were done as single agents, some were done with combinations. And it really wasn't until later in the mid-2000s that we started to see the adoption and incorporation of biologics into this kind of Q. But if you look across those agents that you can see there on that list, you can see that, you know, most of them have very modest efficacy. There were a few kind of winners that we kind of looked at a 12-month survival rate of 30%. Think about that, 12-month survival, 30%. So, not a high bar, but you can see the ones that kind of touched it were basically fell into that line of alkylating agents like platinum and the cytotoxics like Paxil and Topatikin. And so, we started to take this kind of screening procedure and move them into an earlier line of therapy addressing patient population and need. And so, there was this kind of iterative process that took now, you know, over 35 years of bringing these drugs into the clinic. And so, I've listed here are kind of the timelines for the adoption. First, you know, I spent about a decade exploring the platinum analogs to get us to basically say that cisplatinum by itself was probably just as good a drug as any other. And it didn't really matter if we changed the infusion or dose or if we, you know, adopted other analogs at the time like carboplatinum. We basically got the same kind of efficacy outcome of that. So, then the next thought was then to, well, let's start moving it into combinations. And you can see that over the next decade or two, we started to move through a series of combination trials. We added a third agent. We added, you know, non-cross-resistant agents. And we started to focus then based on that 127, 227 series that I just showed you, the types of doublets that maybe were the most promising. And of course, Paclitaxel and Topatican entered into that scene. And you can see now, you know, 15 years ago, we were, 15, 20 years ago, we were already working with Paclitaxel doublets. And then Topatican ultimately got approved in the United States for its combination with cisplatinum for advanced metastatic cervical cancer. And so, I've kind of listed here, you know, our target was a 30% one-year survival. And you can see back in the 1985, the median, it would be the 50% survival was at seven months. And by the time we got to 2009, you know, more than two decades later, we were up to just over that 12 months. So, we had focused on trying to increase overall survival to from 30% to 50%. We kind of got there with GOG204, and that was the kind of the combination that went forward. So, then we started to look at what we had in our, what we call the bullpen. So, for those of you who are baseball, American baseball, this is, the bullpen is kind of where we see the pitchers that are going to be coming in, and they get warmed up when the pitcher that's on the mound starts to wear out or starts to do some crazy stuff. And so, we'll pull people from the bullpen as they warm up. So, while we were doing these chemotherapy trials, we were investigating these other kind of aspects. And you can see they're all targeted towards biological issues. On the left-hand side, you can see angiogenesis. You see immunotherapy in the middle, and this antibody drug conjugate, which is focusing on the expression of a specific antigen on the surface of the cancer cell. To provide a potential homing mechanism to bring a cytotoxic agent. And so, the first of these that we investigated were the biologics. So, as many of you know well, one of the hallmarks of that transition between a low-grade and a high-grade intrapithelial lesion are the vascularity of the tumor that you can, of the lesion that you can see by colposcope. And so, we knew that vascularization of the tumor was going to be an important aspect for cervix cancer. This was then shown in a single agent with Bevacizumab in that same kind of cue that I shared with you earlier, and ultimately was brought into this trial design, which was a true bifactorial design. So, two of these arms are chemotherapy-related. One was paclitaxel and cisplatinum. One was paclitaxel and topatechin. So, a non-platinum-based regimen. And then, two of these arms were in the presence or absence of Bev. So, there were four arms equally randomized one-to-one in a bifactorial design. And so, it was an elegant study design to address a number of questions. You can see that the patient population involved were largely squamous cell cancers, but you can see that the heavy preponderance of the patients enrolled in the trial were patients who had recurrent disease, or had persistent disease following frontline therapy. So, the de novo patient who presented with, let's say, lung metastasis was a minority. So, this was a patient population that had either had previous treatment with recurrence or had persisted through their frontline therapy. And you can see most of these patients had seen platinum, and many of them had pelvic disease. And so, this was published in New England Journal of Medicine in 2014. The first analysis that we had in this study was that there was no significant difference between the chemotherapy arm, or that there was, you know, potentially some difference in the chemotherapy arms, but they were able to be collapsed because of how they performed. And so, the primary result was to look at the chemotherapy combined arms versus the chemotherapy combined arms plus Bevacizumab. And so, what you're looking at on the left is the overall survival endpoint, and on the right, the progression-free survival endpoint. And you can see that in both of these scenarios there was a statistically significant improvement in both of those survival time and event endpoints of about a 30%. Now, I always like to highlight the hazard ratio represents a risk of reduction for an event at every single point of time and exposure. So, while we focus a lot on the medians, and you can see there's about a four-month difference on overall survival, three-month difference on PFS. What really is impactful to patients is that the likelihood for a death event or a progression event is actually reduced by 30%. And that's how you interpret a hazard ratio in a clinical trial like this, that at every time point, even at three months into treatment, the likelihood that the patient will die or progress is going to be reduced by 30%. And it stays that way proportionally throughout the exposure. So, it's a very impactful endpoint and observation. And these are the individual dosing curves. So, you can see paclitaxel and platinum plus or minus bevacizumab here and paclitaxel and topatecan plus or minus bevacizumab here. There isn't a statistical difference in the topatecan arm, but you can see that both of the curves basically separate demonstrating the efficacy of bevacizumab in the setting. So, if I add this to this graphic I shared with you just before, you know, I showed you that we basically went from seven months to 12 months, 50% in that timeframe with the chemotherapy combinations. And when we added bevacizumab, we all of a sudden then jumped up by another 50% in our expectation for overall survival, where now we're approaching 17-plus months in overall survival in patients getting this triplet. So, the next in this, of our arm materian was the immunotherapy. As that data started to emerge that this member, this is a virus, okay, and the body takes care of viruses by educating itself against those viral antigens and then educating the T-cells so that they have that efficacy to remove that infection. So, that antigen presentation happens in the lymph nodes peripherally largely guided by CTLA-4, and then gets educated in the periphery by PD-1, PD-L1. And under normal circumstances, to avoid overstimulation of the immune system, there is blockage of this through the PD-1 pathway, which can stop the immune angle. So, we learned that cancer cells can understand this signaling and can escape immune surveillance by expressing PD-1, PD-L1. And so, our ability to block that either at the effector site, so the T-cell around the tumor itself by the ligand, that we were able to allow for an immune surveillance event to happen, ultimately hopefully killing the cancer cell. And so, we had a number of trials that were done looking at immune checkpoint inhibitors, which obviously were prolifically being studied in other tumor types like melanoma, bladder, lung, and adopted that to this infection that we saw in the cervix that undermines, underlies cervix cancer. And you can see that in this study of about 100 patients, of which, most of which expressed PD-L1 on the cancer, we did, were able to shrink the tumor. So, while the 14% response rate isn't earth shattering, what is more earth shattering on the right-hand side is that, is the number of patients that did not have relapse for many years. So, this was something we never saw with chemotherapy. Now, we're starting to see this unusual response to these patients having very durable long-term responses. And of course, that was persuasive to the FDA to provide for accelerated approval, ultimately leading to our ability to add this to our most successful chemotherapy combination, which was paclitaxel cisplatinum and bevacizumab. So, kenode A26 was birthed in that patient population to try to evaluate the efficacy of adding a PD-1 inhibitor in this case to the backbone of a chemotherapy agent with or without bevacizumab. So, bevacizumab is optional in this trial. And you can see it was used, as I'll share with you here, it was used frequently, not in every exclusively. But you can see here that critical to this, to this particular study was also to evaluate the expression level of PD-L1, which we know is largely expressed in most of our cervix cancers, but you can see here that about 90% of the patients did express some level of PD-L1 on the tumor. And so, this trial was done very elegantly. It's a great paper to read. If you're interested in just clinical trial design and analytics, this is just a cool paper to read from that standpoint. But it's also quite nice to see just how elegantly this trial was done in order to show the efficacy of this regimen. So, what you're seeing here is a step-down analysis done in a patient population that expressed essentially the target for which PEMBRO was intended, and that was these patients' tumors that had high-level expression, if you want to call it that, a combined positive score of greater than one, one or greater in the patient population. And you can see it's a large proportion of the patients, 90%, as I said, and hazard ratio here showing 0.62. So, that's, again, about a 40% reduction in the probability for progression or death at any point along the exposure curve. And because that was positive, the statistical analytical plan then passed the alpha on to the progression-free survival evaluation in the intent to treat. So, this would include those 10% of patients who did not have CPS-positive testing on their tumors, and you can see that even with the inclusion of those patients, the total population had a hazard ratio of 0.65, and yet, again, showing some benefit. And then in the, since that was positive, all the alpha was then passed on to a subgroup of those patients who had expression of PD-L1, and in this case, you can see it's higher, more than 10, which would highlight essentially about half of the patient population that was under study that had high levels of expression of PD-L1, again, demonstrating substantial impact for the use of, with pembrolizumab in this combination with a hazard ratio of 0.58. Now, because that was positive, all the alpha was then passed on to the subgroups evaluating overall survival. Now, surprisingly here, we're seeing a very similar effect. I say surprisingly because we hadn't seen very many studies that had a positive PFS effect that turned into an OS effect, but in this case, we can see it's almost the same magnitude. Hazard ratio of 0.64 in the CPS-positive population of greater than one, of course, passed on to the ITT population, again, positive, and then ultimately, in the subgroup, was highly expressing PD-L1 tumors at 0.61. So, because that was all positive, we passed on the alpha to the response rate. Okay, so now we're looking at which of these actually will accomplish a reduction in tumor size according to Rhesus, and you can see here that the response rate was in that greater than 1% population was 68% versus 50% in the chemo alone population. It was in the outcomer, it was 66%, and in the highly expressing tumors, it was 70%. And interestingly, if you look at the bottom part, these all represent the duration of response curves. So, again, you don't really appreciate this in the PFS analysis because this is only looking at patients who respond, but what you do see is that the patients that do respond, that there is that tail, kind of the immunological tail that we see in certain tumor types being studied with checkpoint inhibitors where you can see it starts to flatten out about 9 to 12 months and stays that way for many, several months afterwards. So, our hope is, and I can't prove this, but our hope is that if a patient never progresses after this point in time, at a certain point in time, their likelihood to progress is going to be essentially the same as the background population, those patients are cured. Those patients are cured. And when was the last time we had a discussion that talked about using systemic therapy to, quote, cure recurrent cervical cancer? It's really eye-opening, and I think it really is a tribute to the science of moving from single-agent chemo to combination chemo to biologics, and now the addition of the immunotherapy. Obviously, a four-drug regimen is going to have toxicity, and these were what was seen. On the green, we see the patients that were treated with pembrolizumab, and remember, some of these patients did not get bevacizumab. So, this is a three-drug regimen versus the, essentially, the placebo group, which would be, again, two to three-drug regimen. But you can see that overall, there was no new safety signals seen with this with respect to the individual compounds. So Bevacizumab as an agent and an immune checkpoint inhibitor as an agent and then the chemotherapy as a backbone for these agents. So neuropathy, we saw myelosuppression but we didn't see anything new that was unexpected or that would detract from the potential efficacy of this regimen. So putting it on this graphic, you can see I had to actually change the scale here a little bit. So we've gone from that 12-month expectation back in 2009 to a now 26-month, 27-month expectation in 2021. Three-fold increase in our expectation for overall survival from the chemotherapy era. Really an amazing improvement and certainly a credible advance. Now, a third part of this, of our bullpen is the antibody drug conjugates. As I mentioned, this is a novel strategy that is taking a targeting antibody, looking for an antigen on a cell and linking it to a cytotoxic agent that can't really be delivered systemically because of toxicity. And as you can see here, this connection is made by a very critical and critically important linker, which connects these two and maintains the stability in the blood. So kind of the poster child for this, for us in cervix cancer is sodomabvidotin. This was a very strategically developed antibody drug conjugate focused on tissue factor, which is ubiquitously expressed in cervix cancer. And it brings a well-known cytotoxic payload that is accompanying most ADCs in development now, this R-statin analogs. This particular compound links four chemotherapy compounds to a single targeting antibody. And again, this is a fully human antibody that brings chemotherapy through a protease cleavable linker. So that linker is really important because that's how, as you can see in this next slide, this is how the drug actually gets into the cancer cell. So the homing antibody is this IgG-based antibody targeting tissue factor, which is expressed on the tumor cells. You can see there this antigen binding number one in this graphic, basically then allows us to be endocytosed into the cell, brought in context with lysosomes, where the lysosomal proteins will then break down the linker, which then releases the microtubule and poison into the cell. And with this, we see not only cytolysis happen and release of some of that MMAE into the neighboring environment, so-called bystander effect, but we also see that this recirculation of the antibody actually can lead to other antibody-dependent processes, such as ADCC and antibody-dependent cytotoxicity, but also antibody-dependent cytositosis. So this provides not only the specific cancer cell itself, but also this environment that the cancer cell is working in or that it exists in to actually affect bystander cell kill and immune education. So this was brought to the clinic a few years ago. We were fortunate to participate in this trial. It was looking across several solid tumors published in Lancet Oncology in 2019. A large portion of the patients that participated in this trial came from the GYN space. We sent over, this was, we had a big contingency of these patients in MD Anderson, and we sent cervix endometrial ovarian cancer. You know, about half the patients came from that GYN space. And you can see that in bladder and cervical cancer, there was a very high objective response rate in this kind of large basket trial of patients with solid tumors. And we learned a lot in this study. So one is that we didn't really have a good handle on the ocular mitigation strategy. We had some idea of what to do. We didn't really have a good strategy for it, but we learned from it. We were able to address many questions about concerns about bleeding, because of course this is tissue factor. So, you know, that's involved in the clotting cascade. And so there's obviously a lot of concern that this would somehow block tissue factor function. It doesn't. But we learned a lot about that process. And so we set up a trial of a hundred patients that we felt would be valuable to expand this experience in cervical cancer. And so you can see the eligibility was recurrent or extra pelvic metastatic cervix cancer that had progressed during or after doublet-based therapy with Bevacizumab if they were eligible, and had had no more than two prior systemic regimens with good performance status. And the goal was to treat these at two milligrams per kilogram every three weeks until progression around susceptible toxicity. And we use this analysis, a primary endpoint as objective response as assessed by an independent review committee. You can see a hundred patients here, basically fits the histology that we would expect to see. Most of them are squamous cancer. Most of them had metastatic sites. What I want to draw your attention to is the fact that many of these patients had had Bevacizumab in the frontline setting, and many of these patients had not responded to the therapy that they were just on. So a lot of these patients had gone and progressed through that immediately preceding therapy. So 56% of the patients actually had progressed on the prior line of therapy. So very, I think, difficult patient population to treat. And this is what we saw. So very exciting, obviously. 101 patients, 24% response rate. We see seven of those patients had complete responses. The waterfall plot, I think, is really impactful because if you think about how you treat patients, we usually treat them by evaluating them in their response to treatment. We generally don't stop treatment if they haven't achieved an objective response. We generally stop treatment if they've achieved objective progression. So you can see that most of these patients were at least to make it through their first post-progression or their first post-evaluation CT scan, and which is listed here as anything that showed either stability or response. So 80% of the patients, essentially, were able to go on to another course of therapy following that first assessment CT scan. One thing that didn't really surprise us too much was that we didn't see a big difference in terms of tissue expression as scored by this H-score and objective response to the agent. You can see the response rate was basically the same or the proportion of patients based on their expression levels. So really no difference in expression level and the opportunity for response. And the duration of response is listed here, 8.3 months. Again, well outside of what our expectations were for chemotherapy in general. And of course, we're very excited about that and was ultimately considered very impactful to patients. Here's just the nuts and bolts on PFS, 4.2 months, and the overall survival median at 12 months, so 12.5 months. So, and again, another line of therapy later with a 50% likelihood to make it a year. So when we put this in context of all those trials I showed you before with single-agent chemotherapy, the blue line here represents Bevacizumab. So you can see why we were so excited about moving Bevacizumab into the frontline setting because it was outperforming even single-agent chemotherapy. Well, here's what TV does in the same population. Again, showing another step forward for us with respect to prevention of progression in this patient population. Now, our most common treatment-associated adverse events were no different than what we saw in the first-line setting with the exception of one, and that of one major one, that was the conjunctivitis dry eye issue that we had seen in the phase one. We were able to do a better job of mitigating that toxicity. I've listed the three kind of AEs of special interest here to kind of highlight, first of all, what the frequency was and also the grade. And you can see that, like our other experiences with ADCs, that the timing to onset to some of these toxicity, especially ocular toxicity, is very predictable. It's usually in that first or second week of the second cycle. And fortunately, they resolve and resolve quickly and do not necessarily require the discontinuation of treatment. You can see that bleeding, mostly in the form of epistaxis, was present. And this is why we tried to put the cooling pads over the NARES as well. And of course, as with any chemotherapy, like an MRS, an analog peripheral neuropathy would be something to keep an eye on. And this, to me, is more problematic of these because they take a long time to resolve if they do, and do frequently, if they get severe enough, require discontinuation. But you can see that most of the patients who had peripheral neuropathy were either grade one or grade two. And of course, this then led to an accelerated approval for the drug on September 20th of 2021. So those of you may have already had some experience with it, but we were very excited to see this now added to our armamentarian. And of course, that's gonna be requiring a confirmatory trial called Innova TB 3301 or GOG 3057, which is accruing right now. And hopefully we will confirm the efficacy of this drug, TB, versus investigator choice chemotherapy, single agents in that patient population that we just saw. So I think with the kind of take-home message here is that these three components of biology really have helped to advance the science in this space. And we're very excited that they are continuing to evolve. Obviously, TB being an active single agent puts it at a prime position to look at combinations. And so we've added this with bevacizumab, with the PD-1 inhibitor pembrolizumab, with chemotherapy. And you can see these are being done in this expansion trial, Innova 205 or 3024, GOG 3024, looking at this in various different settings, including previously unexposed patients, previously exposed patients, and different schedules. And this RMH down here at the bottom actually kind of represents the pinnacle of this, which was to look at the replacement of paclitaxel with TB in the 826 kind of combination. So this is chemotherapy with TB, plus or minus pembro and bev. Now we have some preliminary data on these combinations. I'll just share with them briefly here because they've been presented at ESMO. First was to look at this in combination with chemotherapy. So you can see this is in first line setting. So the response rates were actually quite impressive, 55% with the 12% complete remission with most patients getting their anticipated therapy. Again, the side effects, again, relate to the specific drugs themselves. We saw no acceleration of the ocular toxicity. In combination with pembrolizumab in the second or third line setting, we see a response rate of 38%, again, small study, but these are, again, trying to provide the support for this use in earlier lines of therapy as a combination. You can see that, again, the ocular toxicity around 50%, most grade one, two, as just as we'd seen before. And again, in this particular setting, also looking at these immune adverse events and those that need to be monitored. So overall, we feel very confident that this development strategy with this novel new set of toxic will be able to continue to advance the science and add to this spectrum of drugs that we're now looking at across the portfolio. I think if we'd given this talk a couple of years ago, we'd have very few of these splatters on this target zone because there was very little interest in developing in cervix cancer. Fortunately, with our experience with the novel compounds of immunotherapy and antibody drug conjugates, there's renewed interest to explore this space, and we're very excited to see this as we go forward. So I think you could agree with me that we've made significant and important progress in life expectancy of patients with advanced stage cervical cancer, particularly in that second-line setting. Obviously, there's gonna be challenges that will continue to plague us with respect to exposure, to access, to cost. We do think that the immune system, particularly immune system education is gonna be most impactful for long-term, durable remissions, and who knows, maybe even some cures. But we're not there yet, and so our goal is to continue to work on both ends of the spectrum. First is to look at these new therapies, expanding our ability to leverage more novel therapies in that setting, but also to work on the prevention and early detection so that we can prevent this from ever being a part of our needs. So again, I wanna thank everybody for joining us today. Gonna stop my sharing here. There we go. And happy to address any questions that may be percolating through. Let's see here. One of the questions is, what about Pembro in first-line setting or in stage two and beyond? So this is a good question, and there is a development plan to look at the use of immunotherapy in combination or around the time of radiation or chemoradiation. So there's an extensive amount of work being done exploratory now, not only looking at PD-1 inhibitors, but also CTLA-4. And I think that there's going, we've learned from other tumor types that there are needs. We need to kind of think about what we are actually treating when we do this type of therapy. So not only the agent in hand, but also what is the exposure? So if you remember, I said that a lot of the immune education happens initially from antigen presentation in the periphery. So if we're radiating the periphery and killing out the nodes there, do we have the same degree of successful immune education in that space? And is PD-1 actually the right drug to use? So these are kind of questions that are being assessed and being addressed. We may be seeing a change to neoadjuvant, the role of neoadjuvant therapy, or an adjuvant setting. And of course those trials are ongoing right now. So we have trials that are ongoing to evaluate all of those questions. So neoadjuvant, concomitant, and post. You may have heard about the CALA trial, which was, we haven't seen the full data set yet, this was a trial that was trying to look at adjuvant post-chemo radiation therapy for immunotherapy maintenance surveillance. And that unfortunately did not meet its primary endpoint. So there's a lot more work to be done with that space. Good question about second line therapy for small cell. Boy, that's a tough question. There are not a lot of really effective novel regimens in small cell. What we have been doing with small cell is next-gen sequencing to try to understand whether or not there are other therapies. Small cell is a broad category of tumors. And there are some tumors that fall into this small cell environment that do have targetable alterations that potentially could be leveraged. In the absence of that, yes. We generally, for patients with small cell carcinoma, throw everything at them. Chemosurgery, radiation, and chemotherapy for early stage. Obviously, chemoradiation for a tumor that can be amounted within an environment. We do not have evidence about adjuvant therapy, which is another part of this question is, what about adjuvant atopsitis platinum? We don't have any formalized data that would suggest that that's different than not treatment. But I think if you're concerned about the quality or the completeness of the radiation, I wouldn't be opposed to it. We just don't have any great strategies for this very difficult disease. One question came in about, can you give it to a PD-L1 negative patients? Well, in the United States, you can't because that's a biomarker. We do have data on the efficacy of the combination regimen in patients who were, this is in keynote 826, who were PD-L1 negative. And we did see some efficacy there, but it's hard to point that out as a specific event for the immune therapy. In the single arm therapies, both for pembrolizumab and some of the other PD-L1 inhibitors that are being evaluated, the response rates have been low in PD-L1 negative tumors. And it could be more a reflection of the responses seen in those patients with single agent immune checkpoint inhibitor that it came from old sampling or old testing for PD-L1. So it'd be one thing to look at maybe contemporary biopsy to see if that patient is truly negative, but the likelihood of a response from the single agent therapy is actually quite low. Okay, I don't see any other questions yet. So I don't see any more questions. I guess that we'll kind of conclude. This is again, a great pleasure to be with you today to talk about cervical cancer and the efficacy that we've seen with this introduction of this new drug, this introduction of these novel treatments. I would certainly like to thank Sijin who's been supporting this webinar. The recording from today's presentation will be on the IGCS Education 360 Learning Portal in a couple of days. And so information about IGCS education can be found there, including information about the final IGCS Advances and Updates webinar for 2022, which will be Overall Survival Data with PARP Inhibitor, Myth versus Reality. And super good one. This is gonna be given by my good friend, Dr. Mansoor Mirza, obviously somebody who's very close to this PARP space. And so it'll be a good time. We're gonna talk about more about that in the coming 2023 as well. So this might be a good way to tee up that discussion. And then hopefully when we get together again in Seoul, we'll be able to address this even more so. So once again, thank you so, so very much for joining us today. And I hope you have a great rest of the 2022. Take care.

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