Good afternoon again, everyone. Welcome to the next session with Immuneering. I'm Ami Fadia, Biotech Analyst here at Needham, and it's my pleasure to be hosting Benjamin J. Zeskind, who is the CEO of the company. Benjamin, thank you for taking the time today. If I could request you to kick us off with some opening remarks and priorities for the company, and then we can dive into more questions. Sure, that'd be great. Well, thank you, Ami, and thanks to the entire Needham team for having us today, and thanks to everyone for listening. 2026 is off to an exciting start for us. In January, we reported nearly double the expected overall survival at 12 months in first-line pancreatic cancer. That's something no other therapy has shown in the first-line setting. We explained why, right? I think every other treatment is really designed with a single mechanism, which is just to shrink tumors as quickly as possible right now. I think that the limitation of that strategy is you ultimately get resistance and escape. The tumor may shrink for a while, but ultimately comes roaring back worse than before. We designed our drug, atebimetinib, really with three mechanisms. Number one is to also shrink tumors, but to do it in a much more long, slow, steady, durable way, where we're not driving on pathway resistance in the same way. That's really the first mechanism. In parallel with that, we also designed it to preserve body mass, to help patients maintain or gain weight. Normally, patients in pancreatic cancer lose weight, and that's really about counteracting cachexia, this molecular mechanism by which tumors, particularly in pancreatic cancer, can cause patients to lose weight. The third mechanism is really around minimizing side effects. I think we've shown that consistently. We designed this drug to really drive as few side effects as possible, and that really helps support survival. I think that's been shown in the literature, and certainly, we believe that each of these three mechanisms together is helping to drive the survival that we're seeing, and essentially keeping patients stronger keeps them alive longer. That's really what we've shown to date, and I think the rest of the year is going to be really exciting as well. Right? Next week at AACR, we're showing data around the acquired alterations in circulating tumor DNA, which again, speaks to the mechanism, how we don't drive on pathway resistance in the same way. We've guided to another update on survival in the first-line setting in pancreatic cancer in the first half of this year. We've guided to dosing the first patient in our phase III study in first-line pancreatic cancer midyear. We've guided to dosing the first patient in our lung cancer study, our phase II, in combination with Regeneron's anti-PD-1 Libtayo, and we've guided to dosing the first patient in that in the second half. Really an eventful year coming up for us. Yes, it sounds like it is indeed going to be a busy year for you. Maybe just to put the mechanism in context, you talked a little bit about some of the key aspects of the disease that you're trying to impact with the drug, but maybe if you could just give us a little bit more background on what the Deep Cyclic Inhibition, which is very fundamental to the mechanism of the drug, is meant to do, and how is that different from a lot of the MEK inhibitors that we've seen in the past? Sure. Absolutely. The traditional approach to targeted therapy, whether it's inhibiting MEK or inhibiting RAS or another target in this pathway, it's really been all about chronic inhibition. It's been about making drugs with long half-lives that shut down the pathway 24/7. That does a really good job of the thing that most people look for, which is how quickly do you shrink tumors in the moment. That's a lot of what's measured, certainly pre-clinically and in the early stages of clinical development, right? It's all about what percentage did the tumor shrink at their best, right? That's fundamentally what an overall response rate is. It's sort of what was the best possible moment for a tumor. It's sort of like a 52-week high for a stock. That's what ORR is. It's like the best possible moment. What we appreciated, really from the beginning of when we started this company, is that that's not the thing that really matters most for survival. What matters most for survival is how durable is that tumor shrinkage. The reasons that a potent, continuous inhibition like everyone else does, the reasons that's often very temporary, have really been well worked out in the literature, including work by Robert Gatenby at the Moffitt Cancer Center. What Dr. Gatenby did is he took Darwinian natural selection theory, and he used mathematical models to apply that to the situation of a tumor that's sort of under the continuous pressure of a typical sustained inhibitor, like a MEK or a RAS inhibitor. What he found is, quickly, with that selective pressure, you end up wiping out the population of sensitive cells. Cancer has a high mutation rate. There's millions of cells in a tumor. There's always either already or they're evolved to be a small subset of cells that are resistant, and they take over, and the tumor comes roaring back worse than before. What Dr. Gatenby showed is that it's actually better if you can sort of keep the sensitive and the resistant cells fighting with each other. That's really what Deep Cyclic Inhibition does. We have intense pulses of inhibition. Now let me take a step back. For the patient, they just take an oral medicine once a day. Everything I'm about to describe to you all happens in the chemistry. For the patient, it's just as simple as can be, an oral medication once a day. What's happening within the patient, because of the novel chemistry of atebimetinib, of our Deep Cyclic Inhibitor, is that the drug spikes really quickly to a very high concentration. It's called a high free fraction Cmax. It hits the tumor hard. It's well above the IC90. It's shutting down the pathway more than 90%, almost completely. Because the drug has a fast off rate, it detaches from the target and has a short half-life, so the concentration drops in the blood. The result of that is basically a complete release of the pathway by the end of the day. What that does is it causes the tumor to essentially let its guard down. It goes straight back to using the MAP kinase pathway, and the next day, we hit it again just as hard. For those two populations that I described within the tumor, the sensitive and the resistant cells, they're essentially seesawing back and forth. They're fighting each other, rather than fighting the patient, if you will. To paraphrase Abraham Lincoln, "A tumor divided against itself cannot stand." Right? That's what we're doing. We're causing a civil war within the tumor between the sensitive and the resistant cells. That's really the first mechanism. That's how we get the long, slow, steady, durable reductions in the tumor, because the populations fight each other, and eventually you kind of whittle them both down. The second mechanism is really, as I mentioned, around preserving body mass, counteracting cachexia. There, we've reported 84% of evaluable patients in our phase II in combination with chemo and first-line pancreatic cancer. 84% of them are stable or gaining weight. That has to do with the way we inhibit MEK, which blocks this cachexia mechanism, which is how tumors generally eat away at a patient's muscle mass. We block that. That's the second mechanism. The third thing is this pulsatile inhibition. The other beauty of it is it leads to much better tolerability that we've reported so far. The reason for that is healthy cells need the MAP kinase pathway, too, right? We have this pathway for a reason other than for cancer to hijack it. If you just shut it down 24/7, like most targeted agents do, and whether it's RAS or MEK, you get a lot of side effects. They're on-target side effects, right? It's taking away the pathway. Whereas with this Deep Cyclic Inhibitor approach that we're using, the healthy cells and the malignant cells both need the pathway, but they need it a little differently. The healthy cells need it intermittently. They need it every now and then. The malignant cells need it on all the time. With this pulsatile approach, essentially we're depriving the malignant cells of the sustained high level of that kind of signaling that they need, but we're giving the healthy cells the pathway once a day. That's why we see, we believe, such good tolerability. It's really all three of these factors together that support the patient's survival. If you look in the literature, patients with pancreatic cancer who lose weight have a hazard ratio of 1.55 relative to those who are stable or gaining weight. Losing weight actually contributes to worse survival. By counteracting cachexia, that's a distinct mechanism that we believe one of the reasons atebimetinib is helping to support survival. Similarly with the side effects, in the literature, when a patient's performance status declines to ECOG 2, similarly, it's a 1.48 hazard ratio. When patients can't get out of bed, they can't work, they can't take care of themselves, which you imagine is a lot more common when they have a lot more serious side effects. I think we've all seen that unfortunate kind of spiral that happens. The other thing is, when patients can't go on to a second-line therapy, the hazard ratio there is 1.51. If they're so beat up by side effects that they can't go on to another therapy, that also increases the risk of death. What we think is so unique about Deep Cyclic Inhibitors like atebimetinib is that they're really supporting survival with three distinct mechanisms, as opposed to everyone else that really just has that one mechanism. Yeah. That's interesting. The other aspect that I wanted to really elucidate here is try and understand why we've seen maybe a meaningfully better response in first-line patients than second-line. Of course, we saw activity in both. In first-line patients, we are seeing maybe an even more dramatic improvement in the efficacy outcome that you've reported on so far. Help us understand how that treating the patients earlier in their sort of disease makes more sense with this mechanism. Yeah. I think it's primarily due to the fact that we've prioritized the first-line setting in our studies, right? We've done this for a very simple, clear reason. That's where the most patients are in pancreatic cancer. There's twice as many patients in the first-line setting in pancreatic cancer as in the later-line setting. Sadly, many patients don't make it out of the first-line setting. That's been our priority from the start. That's where we really focus, that's where we've run the phase II, where we've reported the results in January, where we saw this really extraordinary survival. To do that, you really have to combine with chemo. That's what we did. We combined with chemo in the first-line setting. That's what patients expect, that's what the doctors are used to doing. Because we're so well-tolerated, we're able to very readily combine with chemotherapy. I think the reason the majority of our data is in the first-line setting is because that's really what we've prioritized. That's where we're seeing just such incredible survival, because we've been focused there, where we reported in January the 64% overall survival at 12 months, where the benchmark for standard of care, gemcitabine/nab-paclitaxel from the pivotal study, that study, the MPACT study, was 35%. That's really why we prioritize it. I guess the other point I'd make is, with first-line chemotherapies, the primary resistance pathway is the MAP kinase pathway. I think that's really an important fact to remember as you think about second line versus first line. Arguably, the dynamics are just very different there. I think in second line, there was a poster at AACR a couple of years ago out of UC San Diego, where they showed that a lot of these first-line chemotherapies actually can sensitize cells to RAS inhibition. It makes it interesting to think about those dynamics. Got it. Okay. You sort of gave us some data points on the data that you've announced from your phase II-A so far. We're expecting another update in the first half of this year. Maybe if you could lay out what data points you will be sharing at that update, and particularly with regards to overall survival, what do you see as the benchmark? Yeah, absolutely. I guess I have the slides, might as well show you. This is what we announced in January, right? This is the survival that we've seen to date. This was, as of that data cutoff, with 13.4 months median follow-up, so time. Median overall survival not yet reached. 64% overall survival at 12 months. As I alluded to, when you plot the cross-trial comparison with the pivotal studies from standard of care, gemcitabine/nab-paclitaxel, I think what's so encouraging is not only do the curves separate early, but that they separate very consistently across six months, nine months, and 12 months. We shared updates, as you know, at each of these time points. The upcoming update will be our fourth survival update in the first-line setting. I think we've been very communicative, transparent about the progress and the survival that we're seeing. This is in 34 patients, and our original goal for this study was to enroll 30 patients. We enrolled 34. The demand from our sort of additional slots was just so high that we ultimately took another 20 or so patients. The update that we've guided to in the first half is really from that expanded cohort of more than 50 patients. This original 34 plus another 20 or so over 50 patients. Now, because those 20 or so started later, it pulls the median follow-up time a little bit earlier. That's why we wanted to give it a kind of a little more time, and now in the first half, we've guided to sharing those data. That'll be a survival update on a larger cohort of patients. We're really looking forward to sharing that. As we alluded to in January, the OS in the expanded cohort trending consistently with the OS in the original 34 patients. What does that mean for the data points that we might expect to see, because like you said, it sort of pulls forward the median follow-up time because these additional 20-some patients started later in the study? For the larger cohort, I suppose we might get an updated survival rate at whatever that median time point is. Should we expect that we will not get the median OS at this point, given where we are with kind of the larger cohort? I think we'll save any details for the update in the first half. We really won't have long to wait for that update. Yeah, I can't go into really further details about it right now. I think the kind of things that people will be looking at, certainly the survival data, I think certainly some of the secondary endpoints. In January, we reported progression-free survival about three months better than the benchmark for standard of care. That was certainly very encouraging to see as well. We reported just really excellent tolerability. You can see the tolerability that we shared in January, only two categories of adverse events at the Grade three level in more than 10% of patients, neutropenia and anemia, both of which are really associated with the chemo that we're combining with, and neither did we see in monotherapy. It's really hard to say that atebimetinib, if atebimetinib is adding much of anything in the way of harsh side effects on top of what you would expect from the chemo alone. By the way, we did all this in an older population, to be able to show this kind of survival in a population where the median age was 69, whereas the pivotal studies that we're comparing against, the patients were in their low to mid-60s, half or less were over the age of 65. I'm sorry, half or less in the pivotal studies were under the age of 65. For us, more than two-thirds were over the age of 65. Again, just the fact that we were able to show this kind of survival in a meaningfully older population, I think these are all factors that I think really made that January update quite robust. Yeah. One of the questions we often get about the space and in the context of atebimetinib is the competitive landscape. The one asset that everybody else is watching is Revolution Medicines data. They've shown some data in first-line, and we're waiting for additional updates from them as well later this year. Maybe just based on what we know so far, how would you compare where atebimetinib stands? As we fast-forward, how do you see this space evolve over time once both you and Revolution Medicines continue to make progress and generate more data with your assets? Yeah, I'm glad you asked. Look, we welcome everyone working in this space, right? This is a terrible disease, and there's no one drug that's going to solve it. Look, there's finally a glimmer of hope on the horizon, right? Even in first line, you now have multiple phase III studies happening this year. I think that's all good. From the perspective of a first-line patient deciding between different studies in the first-line setting, we've really encouraged our friends at Revolution Medicines privately, we've called on them publicly to really put out more data so that people can really kind of transparently compare these two options. Obviously, with all the caveats of cross-trial comparisons. I think this is kind of how it looks right now. If you try your best to compare apples to apples, it's our drug in combination with chemo compared to their drug in combination with chemo in the first-line setting. The first thing is we're able to do that at full dose, at 320. They have to reduce their dose down to 200. Our January disclosure was 64% overall survival at 12 months. They haven't disclosed it, and we call on them to do so. Please share the overall survival data in first-line pancreatic cancer. I think patients deserve to see that. Our median PFS, we announced eight and a half months, undisclosed for them. Share the data. 84% weight stable or gain, as we said. We don't know that for them. Now, what they have disclosed in the first-line setting is the tolerability, and you can cut it a couple of different ways. They disclose any grade treatment-related adverse events occurring in greater than 30% of patients. So if you compare apples to apples there, we have fatigue, they have it in more. We have anemia. We'll call that even, call that a tie, 41 and 43. We have a rash in 38. They have it in 85, more than double. We have nausea in 35, they have it in 63, almost double. That's the end of our list in that category. Theirs continues. Diarrhea in 68, vomiting in 48, stomatitis, which are mouth ulcers, in 43, peripheral edema, neutrophil count decrease, platelet count decrease, and even alopecia. So this is just a very different tolerability profile. And then if you cut it a different way, Grade three or higher treatment-related adverse events in at least 10% of patients. We have anemia and neutropenia, so do they. That's the end of our list. Their list also includes rash, fatigue, and diarrhea. So really just a different tolerability profile. Now, if you look at overall response rate, we think that really the way to compare apples to apples is to look at the confirmed responses. So if you do that for us, it's 12. For them, it's 15. And then the denominator, they have 40 patients in their study, and somehow through their definition of response- evaluable, it drops down to 31. So, and it's just hard to compare apples to apples with those different definitions. So, really the best way to compare apples to apples is to make the denominator the full ITT safety population. And when you do that, it's really pretty comparable between the two therapies. I think treatment beyond progression is an important factor that can help increase survival. We only did that in 9% of patients. They haven't reported the numbers, but they said it's encouraged. Their baseline demographics are undisclosed. We call on them to put that out. We had older patients, and then, we've shared spider plots, which show some nice durable regressions. I think that would be helpful. The bottom line is when you really strip away all the hype, and you look in first-line setting, and you really try to compare apples to apples, atebimetinib has a lot of advantages, and their program has a lot of question marks right now. Hopefully they'll fill those in. Look, we hope it's great. We hope these numbers are great because that would be great for patients. Patients would really have to weigh whatever numbers they put in here against the increased burden of the side effects. Look, if it's comparable, tie goes to the runner. I think if patients can have similar survival and really deal with a much lighter burden of side effects, I think that would be very attractive to patients in the first-line setting. Yeah. That's how we view it. Again, I think it's great to have multiple companies working in this area, and we welcome all of that. When you compare it side by side, atebimetinib has a lot of advantages, and they have a lot of question marks right now. Okay. Well, thank you for sharing that. One other aspect, and acknowledging that we, as analysts and investors, may not see all the data all at the same time, we probably need to wait to get the overall survival data from both the companies, and which is the ultimate basis or assessment of efficacy of an asset. Yeah. How valuable is median PFS for predicting median OS in this indication? Well, the best predictor of OS is OS. OS is the gold standard. Everything else is kind of secondary. I think particularly when you have a drug with three mechanisms like ours, right? When you have a drug that not only is about shrinking tumors, but is also about promoting weight stability and gain, and minimizing side effects to preserve performance status, right? These are factors that can extend what's called the PPS, right, the post-progression survival. That's the sort of the delta between the median PFS and the median OS, is a way to think about it. PFS is based on, at the end of the day, on RECIST, which is based on sort of an arbitrary 30% threshold. There's no substitute for OS, right? The best predictor of OS is OS. At the end of the day, in particular, when you have a drug like ours that's been designed from the start to promote survival, not just by the one mechanism of tumor shrinkage, but by these three mechanisms, I think survival is not necessarily directly correlated. Look, I mean, we have a great PFS, too. I mean, we reported in January eight and a half months, median PFS, which is a full three months better than the standard of care. Certainly, we like what we're seeing there. I think, at the end of the day, OS is what matters to patients. The beauty of this approach is there's quality of life, right? They're not just surviving, they're thriving. I think, particularly with the interview with Ben Sasse on Friday in The New York Times, Senator Ben Sasse, I mean, what a moving profile, just a really courageous individual for sharing his story. I think that really also kind of shown a spotlight on the challenges, the toll of some of these side effects and really kind of put a human face on that. I think we all in the field of oncology owe a real debt of gratitude to Ben Sasse for having the courage to share his story. Okay. If you could move to the pivotal trial study. Sure. Can you talk about your trial design? To share. What- Trying to get to that slide? Yeah, yeah. Oh, sorry. Okay. I was a little distracted by the video. I can show it if you want. That's one of our investigators talking about our patients. Yeah, we can go to that. Oh, okay. Figure if there's time. Yeah, yeah. This is the phase III trial. Yeah. Perfect. Maybe if you could sort of just summarize, if at all, it is different from your earlier kind of study that you're going to be providing an update on, and maybe just talk about what endpoint would be necessary from a regulatory standpoint for approval. If there's a path to accelerated approval here, what would that look like? Sure. Yeah. This is our study. It's called MAPKeeper-301. It's a global randomized pivotal study, and pretty plain vanilla and pretty consistent with our phase II. Atebimetinib plus the modified GNP chemotherapy randomized against standard of care GNP chemotherapy with OS as the primary endpoint. A little over 500 patients in the study. That's really kind of the design. As we announced in December, we have regulatory alignment. The study is fully funded, and we've guided to dosing the first patient mid-year. We're really excited about this study and I think it's a really nice opportunity for first-line pancreatic cancer patients to consider, especially given the data that we've shown so far. Maybe just give us some preview around the landscape. There is obviously a huge unmet need in pancreatic cancer. How should we think about the enrollment pace for the study? I know you're yet to initiate, but maybe just broad sweep thoughts at the moment. Maybe help us think about what would be the data updates from this trial. I suppose first would be the PFS at sometime in the next year and a half or so. Maybe kind of just talk through what might be the key milestones around this study over time. Yeah. Well, let's just be careful about the language, because you said, "have yet to initiate," and I know different companies use the word initiate in different ways. Our guidance is specific to first patient dosed, and we've guided to that mid-year. I think given that we're reiterating that guidance, I think it's fair to assume that we have done many of the activities. Of course. Some companies would refer to when they say a study is initiated. We are just kind of reiterating that we're on track for that first patient dose mid-year. Mm-hmm. That's really the first thing I would say. Our primary endpoint is OS, right? I think that's kind of what FDA, as recently as the guidance they published last summer, they're really focused around OS as the primary endpoint, is what that guidance was over the summer that was made public. In that guidance, they specifically singled out pancreatic cancer as a disease where OS is sort of crucial. They also made the point that we were trying to make earlier, which is that OS is both an efficacy and a safety endpoint, right? When patients have harsh side effects, that can impact the survival. We really designed this study with OS as the primary endpoint. I know you've suggested some things about timeline with PFS. I'd push back on your specifics around timelines and PFS and really just say what we're guiding to is OS as the primary endpoint and a top-line readout about two years after that first patient dose. That's really how we're thinking about the timelines for the study in terms of what we've guided to publicly. Okay. Fantastic. Now, with regards to the chemotherapy that is going to be used in this combination, aside from GNP, there's also FOLFIRINOX that's used in this patient population. Help us understand what might be the implications around the choice of chemotherapy in light of this study, of course, which you're studying only with GNP. What percent in the real world currently of patients are being treated with one versus the other chemo? Would you study it with FOLFIRINOX in the future? Yeah. In kind of the real-world setting, it's about 50/50. The reason for that is gemcitabine-containing regimens are a bit better tolerated, whereas the NALIRIFOX and FOLFIRINOX, as you can see from their phase IIIs in the green here, they're harsher, but they provide a bit of a survival advantage, right? It's really the difference between that orange line and sort of the red and the green line. Our thesis from the start has been if we can provide substantially better survival than any of them, which is certainly what the data we announced in January suggests, obviously with the caveats of a cross-trial comparison. Keeping in mind, those caveats cut both ways because we had an older patient population in our study. It's sort of this tough fork in the road right now, right? A lot harsher side effects for a little more survival. We said, "What if you don't have to make them choose? What if you can give even less harsh side effects and more survival, right? Have the cake and eat it, too." That's really why we've prioritized gemcitabine/nab-paclitaxel, and that's certainly been our most popular arm, if you will, for that reason. We even used this modified GNP, which is even better tolerated. It's every other week as opposed to three weeks on, one week off. That was studied by Daniel H. Ahn and Tanios Bekaii-Saab at the Mayo Clinic, both investigators in our phase II. They showed what you see in the brown, that basically, there's not a significant survival difference, but you get better tolerability. Again, I think you can tell throughout these comments, our goal has been to really make something, a regimen that's very tolerable for patients. They're not just surviving, they're thriving. Right? We believe, again, that's not just some soft quality of life argument. That has a hard connection to survival. The hazard ratios show it. When patients can maintain their performance status, when they can go on to subsequent therapies, they live longer. All of these decisions we made from the beginning have been about supporting survival by minimizing harsh side effects, by maintaining or gaining weight, and by shrinking tumors in a durable way. Now, all that being said, we do have a phase II arm in combination with FOLFIRINOX, and we have shared some interesting case studies from that arm. We haven't shared aggregate data yet, but this is a patient that actually Dr. Ocean spoke about on one of our calls, Allyson J. Ocean from Weill Cornell, great doctor. This is a patient who on our atebi plus FOLFIRINOX arm has had a confirmed complete response. Obviously that's what you want to see in a patient, especially when you can combine it with improved quality of life and weight stability. Certainly, very encouraging things that we've seen from the cases we've shared in that study. I think the fact that we can combine with FOLFIRINOX is differentiating. At the end of the day, if you can give patients much better survival with much better tolerability, we believe that's ultimately the best thing. Yeah Combination with gemcitabine/nab-paclitaxel. That makes sense. I know we have just under two minutes left, and I wanted to squeeze in one last question around the data that you're going to be having at AACR, where you're going to share some ctDNA data. You have shared some before from a smaller cohort of patients. Maybe just preview for us what we should be looking for from this upcoming data set. Yeah. Again, this is about how we do or don't drive resistance, right? How that differs from other targeted agents. If you look at RAS inhibitors, when they're mutation-specific RAS inhibitors, you generally see acquired alterations in other KRAS alterations. In other words, if it's a G12C inhibitor, you see the tumors acquiring G12S, G12V, right? It's a little bit like blocking one lane of the highway. It helps to slow down traffic, but eventually you change lanes, and you go around it. With pan-RAS inhibitors, it's a little bit like maybe blocking two lanes of a three or four-lane highway. Right? More traffic jam, but the tumors can still get around it. You see KRAS amplifications and BRAF mutations most commonly. What we shared from phase I is that we see very few acquired alterations in the MAP kinase pathway, meaning we're essentially blocking all the lanes of the highway, and we're kind of forcing the tumors onto the side roads, if you will, forcing them to pull off the highway and use other pathways that are less commonly used by the tumors. That's really what we've shown to date, and I think our press release announcing the AACR poster made clear that it's a similar conclusion. Yeah Data set. In this data that we shared already, you don't see much in the way of acquired alterations in the MAP kinase pathway, which we believe is an important part of the reason that we see the kind of reductions in tumors that we see, that we've shared in our spider plots, which are in a lot of patients, these kind of long, slow, steady reductions. That's a real contrast with typical targeted therapies, where maybe you would see a faster, deeper shrinkage of the tumor at first. Maybe it goes down into the 70s. After a few months, because of that selection, that natural selection I was talking about earlier, you select for resistant cells, and the tumor comes roaring back. Whereas because we're maintaining that civil war, that tumor divided against itself, the sensitive and the resistant populations fighting as we deliver the deep cyclic inhibitor, you see in a lot of patients these long, slow, steady reductions, and I think that ultimately, we believe, leads to much better survival than if you just shrink it fast for a few months and get resistance. Yeah. That we believe drives survival together with great tolerability and preserving body mass. Okay. Benjamin, unfortunately, we are out of time, but I definitely will be looking forward to your OS data update, which is probably coming soon. Thank you for the time today and for your time for the Fireside Chat. Thanks for having me, Ami, and thanks everyone for listening.