Good afternoon. I'm Eric Joseph, Senior Biotech Analyst with JP Morgan. Our next presenting company is Terns Pharmaceuticals, and presenting for the company is CEO Amy Burroughs. There'll be a Q&A after the presentation. Just raise your hand, we'll bring the mic around to you. And for folks tuning in via the webcast, feel free to submit questions via the portal. With that, Amy, thanks for joining us. Great. Thank you so much, Eric, to you and the JP Morgan team for hosting us and allowing us to tell our story at Terns. And I'd also like to welcome Emil Kuriakose to the stage, our Chief Medical Officer, who will be joining me for Q&A. So we are passionate at Terns about developing a difference, developing medicines that make a difference in people's lives. We had a transformational year in 2024, and we plan to continue that momentum into 2025, where our focus is what we call our two by two by two. Oh, I forgot to say we're going to be making forward-looking statements, so please refer to our website for more information on that. So we're advancing two potentially best-in-class medicines into unique blockbuster indications and two significant clinical data readouts coming in 2025. On TERN-701, our allosteric BCR-ABL inhibitor for chronic myeloid leukemia, or CML, we have a potential best-in-class treatment in a $5 billion market, early clinical data that supports a differentiated profile, a high probability of clinical and regulatory success with a clear path into the frontline market, and upcoming data in the fourth quarter of this year, which we'll read through to our registrational endpoint. On TERN-601, our oral small molecule GLP-1, we shared a differentiated phase 1 data set back in September for our oral small molecule that is easy to manufacture and scale. We also outlined the distinct drug properties that may enable competitive weight loss and superior tolerability in longer-term studies. Our upcoming phase 2 is designed to support our differentiation thesis and will read out in the second half of 2025. All of this is supported by our strong balance sheet with over $370 million in cash, which takes us into 2028, so at Terns, our efforts are broader than TERN-601 and TERN-701, but in the interest of time, I'm going to not talk more broadly except to say that all of our assets are internally discovered. We have two additional obesity assets that are designed to be used in combination with an oral GLP-1 receptor agonist, our THR-β TERN-501, and our TERN-800 series, our GIPR modulator program, so CML is important to me as I lost a close family member to the disease before imatinib was approved in 2001, and the drug transformed CML into a chronic lifelong condition for most patients. Over the next decade, we had additional active site tyrosine kinase inhibitors, or TKIs, that improved on efficacy but had a worse safety and tolerability profile. These are called active site inhibitors as they bind to the ATP binding site on the BCR-ABL fusion protein. Due to the limitations of these active site inhibitors, almost half of CML patients on these therapies switch due to treatment failure, tolerability, or safety. Allosteric inhibitors such as TERN-701 are more selective than active sites and bind to a different pocket on the BCR-ABL protein. The first approved allosteric, asciminib, has shown that this novel mechanism translates into superior efficacy and safety over active site inhibitors. However, asciminib leaves meaningful room for improvement that we will discuss. As a better allosteric inhibitor, TERN-701 has an opportunity to continue to raise the bar for these patients who want and deserve more. Let me tell you more specifics. Our goal for 701 is to be the best allosteric TKI with clinically meaningful improvements over asciminib in three key areas: greater efficacy through optimized dosing and better target coverage, improved tolerability and safety, and improved convenience. TERN-701 will be easier to administer with once-daily dosing without regard to food for all patients. On the following slides, I'm going to provide you with the data to support our target product profile for TERN-701 as the best option for treating CML. Going back to our three pillars of differentiation, our emerging data to support better efficacy is threefold. First, in preclinical assays, TERN-701 has greater potency than asciminib. Second, improved target coverage through improved PK and dose optimization. Finally, early clinical data showing responses in asciminib failures. On safety, we have begun to differentiate on asciminib with the early data from our phase one clinical study, with no DLTs, no dose reductions, and no AE-related discontinuations. Lastly, we have shown how 701 can provide improved convenience and make it more likely that a patient can stay on their drug in a compliant way for life. Together, these pillars represent a compelling opportunity to surpass asciminib as the best allosteric in CML, and we are already building significant clinical data to support our differentiation. At our next data readout in the fourth quarter, you will have the first look at six-month Major Molecular Response, also called MMR, which is important as MMR is the registrational endpoint and requires time to emerge. With that, let's jump into the CARDINAL trial design, our phase one trial for which we shared exciting data early last month. It's a standard dose escalation dose expansion setup. I'll note two things. First, for the first time, the FDA has allowed second-line patients in a phase one study due to the body of data around allosterics and TERN-701. We also allow patients who have been treated with asciminib. Dose escalation enrolled rapidly, and all doses have completed evaluation from 160 mg- 500 mg. As noted previously, we did not have any DLTs in dose escalation, which enables us to talk to regulators about exploring the higher end of the dose range and expansion. Stay tuned for more details on the doses selected as we begin dose expansion in the coming months. As of the data cutoff in October 2024, our analysis included 15 patients. As one would expect in a phase I trial, patients were heavily pretreated with high baseline disease burden and a median of four prior treatments. Of the six patients who had seen asciminib, we saw both suboptimal efficacy and intolerance as reasons for discontinuation. Despite the heavily pretreated nature of these patients, we saw highly encouraging signs of efficacy and safety. So here's the swimmer plot of the 15 patients with details about their baseline characteristics on the left. As we will discuss, we observed meaningful activity after a relatively short median treatment duration of three months. Remember that I told you it takes time for molecular response to emerge in this disease. 14 of 15 patients remain on treatment. The top blue lanes show the seven patients at our lowest dose, mid-blue lanes the next dose of 320 mg, and the bottom lanes in dark blue is the 400 mg dose. To be efficacy evaluable, patients must have at least two on-treatment assessments performed centrally, which is generally done on a monthly basis. The 12 patients at the lower two dose levels were efficacy evaluable. All 15 patients here are safety evaluable. And let me get into a bit more detail about the data. So this is a standard table for a CML trial, but a bit complex for a CML novice. So let me take a moment to explain it. BCR-ABL transcript levels are a measure of disease burden in CML and are grouped into categories. Responses are evaluated by categorical shifts. In this table, patients with the highest disease burden at baseline are in the column on the right as their baseline transcript levels are 10% or more. Post-treatment levels are listed from lowest to highest by row. Those at MR3 or better are in major molecular response, or MMR. This table shows the baseline and post-treatment categories for the 10 patients with at least three months of treatment or an MMR at baseline who do not have a difficult-to-treat mutation called T315I. Patients in the blue boxes maintain their transcript category over the course of treatment. In the green shaded area, we have two patients with higher disease burden at baseline who achieved categorical molecular improvements. Over such a short period of time and with such a heavily pretreated population, we're pleased to see half of patients maintaining or moving into major molecular response. I would also note that no patients had shifts into a worse response category versus baseline, as represented by the red area in the table. Overall, we're highly encouraged to see a cumulative MMR rate of 50%, a promising foundation on which to build our efficacy differentiation. On the next slide, this shows changes in transcript levels for patients with transcripts above 1%. As shown in the plot, seven of eight patients showed decreases. Seeing these kinds of broad decreases in transcripts is a good early indicator of a drug's activity. There was one discontinuation due to a loss of response in a difficult-to-treat sixth-line patient. I'll highlight that most of the patients had a high leukemic burden with baseline transcripts above 10% and several above 50%. This makes these decreases in transcripts even more clinically meaningful at this early time point. Let's take a look at two patient case studies. This is a 35-year-old patient with eight years of prior CML treatment, including six years on a second-generation TKI before losing their response. Following treatment with ponatinib and asciminib for one year each, the patient was switched to 701 not only due to a suboptimal plateauing of response, but also due to intolerance with elevated LFTs and lipid abnormalities while on asciminib. After five cycles on TERN-701, this patient achieved MR2 and a steeper response without the tolerability issues seen with asciminib. We're very encouraged to see activity like this, and it builds on our conviction in our differentiation on efficacy. For the second patient, we have a fifth-line patient with over 10 years of CML treatment. This patient saw imatinib and all three second-generation active site TKIs before losing their response. After just three cycles of TERN-701, this patient rapidly achieved deep molecular response, which is even better than major molecular response. This deep molecular response demonstrates rapid rescue of a heavily pretreated patient with a high baseline leukemic burden. We believe this activity bodes well for the type of rapid and compelling response that we will see in earlier-line patients. The efficacy signals shared are supported by 701's high potency. In this cell proliferation assay, 701 demonstrated numerically greater potency versus asciminib against BCR-ABL variants, including active site and myristate pocket mutations. We believe this potency advantage, when added to better PK, plays an important role in why we are seeing a rescue effect following asciminib and have opportunity to surpass on efficacy. Turning to safety, I'll give an abbreviated summary of findings. Emerging data were very encouraging, with no dose-limiting toxicity seen across all doses, no AE-related treatment discontinuations or dose reductions, no grade three or greater treatment-related AEs or treatment-related SAEs, no clinically meaningful changes in LFTs, amylase, or lipase, and no clinically meaningful changes in blood pressure, ECG, or other vitals. So one parameter that can be compared to asciminib at this early time point is the incidence of dose-limiting toxicities in dose escalation. Both drugs had an initial evaluation period of 28 days, which is typical in initial oncology trials. This is an assessment of safety based primarily on incidence of treatment-related grade three AEs during this first cycle of treatment. Both TERN-701 and asciminib used similar DLT criteria to assess incidence of DLTs over the 28 days of treatment. As you can see, TERN-701 showed no DLTs through the dose range, while asciminib had multiple non-hematologic DLTs at different dose levels. No observed DLTs throughout the entire dose range supports the potential for TERN-701 to have a differentiated safety profile and to explore the higher end of the dose range in our expansion. Switching to improved convenience, we have shown 701 can be dosed once daily without regard to food. The PK profile on the left supports once daily dosing with linear PK and a median half-life of 8 hours-14 hours compared to asciminib's 5 hours-9 hours. On the right, we have shown no clinically significant difference in exposure when dosed with food, and for comparison, asciminib has a 60% decrease in exposure with food. On both these fronts, we think this can provide improved convenience to the patient and ultimately drive greater compliance and efficacy. So based on the emerging data, we have conviction that TERN-701 could be the best drug for all CML patients and will be the best option for frontline patients. We have multiple programs underway to support rapidly moving towards a registrational trial, including our dose expansion, which will start in the first half of this year. I will note that getting to market is a well-trodden path in CML that is well within our capabilities as a company. The next data readout will be in the fourth quarter of this year, where we will provide data from a larger number of patients and those with longer treatment durations. As discussed, this will include data on six-month MMR rates, which serves as a first read-through to our registrational endpoint in CML, and finally, CML is a large and growing market at over $5 billion in sales today and over 100,000 patients on therapy in the G7. 17,000 patients are newly diagnosed each year. With signs of greater efficacy and differentiated safety and convenience, we think we can compete for a significant share of frontline patients. Beyond frontline, there are 15,000 second-line patients switching to a new therapy. Many of these patients have failed a generic active site inhibitor in the frontline. In those cases, physicians will likely want to switch classes and choose the best allosteric inhibitor. Note that we have already shown compelling rescue effects in our trial of patients who have failed an active site TKI and responded to TERN-701. Overall, we are encouraged that 701 can be the best treatment for CML, regardless of class or line of therapy, and are moving quickly to get to market, so switching gears, I would like to talk about our oral GLP-1 receptor agonist for obesity, so in our first-in-human study, we showed a profile that is well-positioned for additional differentiation in phase two. We showed statistically significant and dose-dependent weight loss over 28 days with once-daily dosing. TERN-601 was well tolerated with unremarkable safety findings despite rapid titration to target doses. We talked about the distinct drug properties that enabled sustained target coverage and a flat PK curve, and we believe that this will lead to a differentiated clinical profile in subsequent studies. We have the potential to be a leading GLP-1 receptor agonist with promising efficacy, tolerability, and manufacturing scalability. We are initiating our phase two trial early in the next quarter, and you will see data from that study in the second half of this year. Let me go briefly through the data so the study leveraged an efficient design to explore a wide dose range from 240 mg-740 mg once a day in the multiple ascending dose cohorts. The study was run at a phase one unit in the U.S. with non-diabetic patients with obesity or overweight. Looking at the PK, we see a differentiated profile that supports once-daily dosing. 601 achieved prolonged absorption at 240 mg and above with a relatively flat PK curve, which we believe will translate to better tolerability in longer-term studies. I will show you next how this translated to efficacy. 601 showed dose-dependent 28-day mean weight loss up to 5.5%. This is on the upper end of the range for single-agent GLP-1 receptor agonists in 28-day studies. The curves were well separated with no signs of plateau. I want to reemphasize how important it is to calibrate our TERN-601 data in the context of the rapid speed of titration over 28 days. At 240 mg, titration was weekly. We saw such good tolerability that we set the titration to every three days at 500 mg and 740 mg. Based on what we have seen, this is the fastest titration conducted in a 28-day study. Our intention was not to optimize tolerability in this short study, but to challenge the tolerability of the drug to inform the next phase of development. Despite the challenge of fast titration, participants in the study tolerated it well and did not have to discontinue or ask for dose reductions or interruptions. At the lowest dose, there was no nausea or vomiting. There were no severe or serious AEs and no clinically meaningful changes in liver enzymes. The majority of GI-related AEs were mild, and overall, 601 was well tolerated with unremarkable safety findings. This suggests the potential for a differentiated tolerability profile in our next study with slower titration. When we compare the results of our 28-day study with those of other oral GLP-1s, we see that no other drug had these tolerability outcomes with a fast titration schema. When we presented the data in October, we talked about the differentiated drug properties of TERN-601 that support our belief in its potential as a highly tolerable agent with competitive efficacy. At a high level, we believe the difference is the relatively higher drug levels in the gut versus the plasma that drives efficacy and avoids the exposure spikes in the plasma that likely cause GI tolerability issues. Turning to next steps, we are initiating our phase two early next quarter. Part A is a 12-week study that will read out in the second half of 2025. It is designed to evaluate efficacy, safety, and tolerability with different titration regimens and inform longer-duration Part B arms of the study. We will be particularly interested in whether slowing the titration can yield a superior tolerability profile with respect to other oral GLP-1 receptor agonists. We plan to have more to say about trial design and expectations for the study as we approach study start early next quarter, so please stay tuned. So I'll begin to wrap up by touching on financials. Terns has over $370 million in cash, which provides over three years of cash runway into 2028 and the ability to reach multiple data catalysts. So 2025 represents an exciting year for Terns. We have two potentially best-in-class molecules into unique blockbuster indications and two significant clinical data readouts in 2025. Each of our programs has compelling phase one data for us to build on in 2025. 701 will have additional phase one data that includes six-month MMR, a read-through to our registrational endpoint, and TERN-601, 12-week phase two readout will provide meaningful data on our differentiation hypothesis. And together, we believe 2025 will be a significant year for Terns as we solidify our competitive positioning and deliver on two transformative catalysts. With that, thank you for your attention. I will turn it back over to Eric for Q&A. Okay, great. Well, we have some time for Q&A. And for those who have questions, just raise your hand. We'll bring a mic over to you. I'll get started here, though, just picking up on the CML program with TERN-701. Actually, just in thinking about practice today, right, where you kind of noted a fair amount of switching from first to second generation TKIs, what drives the decision to switch within the existing first and second generation options? Is it one of tolerability or response? Can you just sort of speak to that? I'll let the oncologist speak to that. Yeah, so Eric, about 40% of patients who are on the current drugs in terms of active site first or second gens switch over the course of their therapy. And of that 40%, approximately 15%-20% is due to suboptimal response or treatment failure, and the other due to tolerability issues, and keeping in mind that both of those can have substantial overlap. And so you're talking about that churn of approximately 40%, and that's really what the allosteric class as a whole can decrease substantially on both fronts by having less suboptimal responses/failures, as we've already seen with the superior efficacy profile, and less switching due to tolerability issues because of the superior safety profile. So as a class, this is in an entirely different category, which is why we think that allosterics are—we're in the middle of a paradigm shift in this disease after almost 30 years with no more than one single class of drug. And now this new class is good for patients in that it's incrementally, in a substantial manner, improving on the efficacy and safety, especially for these patients who start early as newly diagnosed and have to be on treatment for life. So if you imagine going forward that that switch proportion goes from 40% to, say, 20% or lower, that's meaningful in that you get more duration out of these drugs than you do with the active site, which, based on our early differentiation from the only allosteric that's approved, we think that puts us in a really good position to be competitive and to really be part of that paradigm shift going forward. One of the clinical studies would say that getting to response MMR, right, can be a function of time depending on the molecule. I guess, how long of treatment is typically followed before arriving at a suboptimal response determination? It's a great question, and the answer is really depending on where you are in your disease. So if you're in multiply relapsed patients like we are in our phase one, there's a highly variable rate of achievement to MMR depending on what your starting point is. And in those patients who are at the highest end of the baseline transcript level, in other words, greater than 10% with multiple prior lines of therapy, as was shown with asciminib, including several other 3G active site TKIs, those patients take the longest in the relapsed refractory setting to get to MMR. And by six months in that subset, it's less than 5% of patients that get to MMR. Then, as you lower that baseline transcript to the one to 10 category and less than one, those numbers go up at six and 12 months. In contrast, in frontline, it is a much faster decrease, even across the old transcript spectrum, which is exactly why in newly diagnosed patients, the ELN guidelines and even NCCN has recommended certain treatment milestones. By six months, most patients should have reached 1% or lower, and by 12 months, they should have reached MMR based on ELN guidelines. Frontline patients have much more homogeneous disease in terms of clonality and biology, where you can set very precise milestones for getting to these important response metrics. And that's why when Amy said it takes time to get to these endpoints, it's more in the context of a more heterogeneous population in the relapsed refractory setting that you need more patients and you need more time, especially for those higher transcript patients, to get to that readout of six-month MMR compared to a frontline where it's much faster. So if you then translate that to what that means for a registrational program, when you're going into second line versus frontline, that's precisely why six-month MMR is the readout. And so it's a very rapid time to your primary endpoint in an early line population in contrast to a much later line that you would see in a phase I population. Does that make sense? I have a question here. Rune Vestermark, Nordic Bioscience, Copenhagen, Denmark. Thank you for a great presentation. If this is in the public domain, I apologize for a stupid question, but in terms of the FXR, THR-beta for MASH, you had positive 2A data as far as I remember. Can you speak a little bit about why we don't see you progressing in that direction? Yeah, so we talked last year at JP Morgan about we had positive data the year before, and we talked in January 2024 at JP Morgan. It was really a capital allocation decision given the cost to move forward in NASH. The upcoming at that point, resmetirom approval without a biopsy requirement and the need for a paired biopsy study takes tremendous resources. And with the priorities we just told you about, we decided to prioritize what we're working on today over committing to an expensive NASH program that would be difficult to enroll with the biopsy study. Thank you. Just coming back to CML, this is obviously an indication where we've seen Novartis innovate time and again doing it with Scemblix here, and they've had a lot of success where others have not replicated to the same degree. Talk about sort of how a smaller biotech can kind of go up against the behemoth in this indication. What does it take? Yeah, I'll let Emil add to this, but I think it's actually a great indication for a small biotech. And actually, originally, it was not Novartis' drug, imatinib. So it's actually an indication where even the pivotal trials were a fairly reasonable size. So historically, they've been about 250 patients for like a second line trial and about 400 for a frontline trial. The need for reps probably in the 50 to 100 scale. So it's actually something that's very doable for a small company. Emil, do you have anything to add to that? I'll just add to that there have been small companies that have taken drugs to the finish line area, being one example with ponatinib. And when you look at in the context of CML compared to other indications in oncology, I think CML is really unique in terms of the registrational program and the requirements that you need to get to. This is probably the only, if not the handful of indications in oncology where response rate remains the regulatory endpoint, no matter what line of therapy you're in. And so in contrast to other indications like lung, et cetera, et cetera, where you may get a response rate-based accelerated approval in relapse, but you always have to do a time-to-event PFS or OS study. That doesn't apply in CML because these surrogate endpoints in terms of MMR have been so validated in terms of the prediction towards longer-term outcomes. So that's really unique, and that's really prosecutable for a small company like us to get to those very short-term readouts in the context of a study in the second line and even frontline. The time to readout is 12 months. And to Amy's point, the numbers that you need to show that differential in response rate are not very high. I'll also add to that a question we often get from investors is, well, don't you need to go head-to-head with asciminib in the frontline? And we do not. Given that the first and second generation drugs are good drugs, we expect that they will continue to be used. They're generic. Due to that, we can do a similar trial as what Novartis did in ASC4FIRST and go against first and second generation TKIs, where we have a high degree of confidence that we will win. In terms of a sort of market positioning standpoint, notwithstanding not necessarily needing to do a head-to-head with asciminib, just the ultimate goal is to compete largely in the frontline setting or kind of be, well, yeah, I guess ultimately sort of what is a competitive profile do you think to compete with Scemblix in the frontline setting at the end of the day? Well, I would say that our target product profile is to be the best in terms of efficacy, safety, and convenience so that when a physician is choosing an allosteric, that they choose TERN-701. We believe that it will be the best therapy for frontline patients, as frankly, asciminib is today. And there may be physicians who choose for cost reasons a first and second generation TKI. As Emil outlined, there's often switching. And so the second line population, once a patient fails a first or second gen active site TKI, the right choice will be to change classes to an allosteric. And TERN-701, we aim for that to be the best choice. Again, safety, efficacy, and convenience. Maybe just pivoting to TERN-601 for obesity, just with the, as you're conducting the 12-week study, right? 12-week study this year, where you have a better assessment of not only the dosing scheme, but also the tolerability profile associated with that. I mean, I'm sure you get this question a lot, right? Investors asking to try and differentiate on the tolerability side or the signal that would support a differentiated tolerability side. Maybe just sort of orient us around a little bit in terms of the GI severity that's kind of observed in the landscape currently and sort of what either based on patient or physician feedback, what would be viewed as a much easier, manageable, better tolerated profile? Yeah, I'll start and let Emil add to it. So we're not guiding to specific numbers on that for phase two, and again, stay tuned as we put out our trial design, and we will guide to additional specifics. I think it's well known that whether we're talking about injectable or orals, there are high rates of dropout or adherence and compliance in the commercial market, and that these kind of first drugs are not really hitting the bar that physicians and patients are looking for in a drug that patients are expected to stay on for the rest of their life to gain the benefit. And so when you look at AE rates of 50%, when you think about living with nausea and other GI-related concerns, and we talk to physicians, they say, "We're not so focused on 7% or 8% weight loss in 12 weeks. We care much more about that tolerability, our patient's ability to stay on the drug, and frankly, our ability to prescribe it in a way that makes it easier for us. We don't want patients calling, asking about titration, asking about how to manage these side effects. And so that's really what we're aiming for. And we didn't talk much about the titration scheme, but we believe that we can have a much simpler titration scheme with fewer steps. Okay. Yeah, and I'll just add that the data that we saw in our 28-day phase one gives us conviction for us to really set a very high bar on differentiation at 12 weeks. And the reason specifically, Amy alluded to some of that, is that the tolerability profile we saw in the 28-day study, specifically with regard to the observation of no dose interruptions, no dose reductions, or discontinuations, despite the fastest titration in any 28-day study that's been done, gives us real confidence that even going to a standard titration schedule, which in every 12-week study has been weekly to biweekly, should dramatically improve that incidence, which, by the way, was not really different from other 28-day studies that titrated much slower, while getting to the same high-end weight loss that other drugs have shown in 28 days without a plateau in the slope of the weight loss. So everybody always focuses on the highest dose weight loss achieved at 28. But even if you look at our 500 mg and the 250 mg doses, they achieved. 500 got to about 4%, 250 got to about 3% with linear slopes and really good tolerability profiles. And so we see an opportunity therefore to be able to slow that titration down in a 12-week study where if you imagine that improving the incidence of GIEs to where we can now set a high bar to be numerically lower than what the other drugs have shown who have had to maintain the same titration schedule from phase one to phase two, that's really what gives us a real strong conviction that we could set a high bar on the tolerability front and set a high bar on simplifying titration to where if we go to 500 and only need two, three steps to get there, that's much easier for patients and much easier for physicians. Both those aspects will be very differentiating, even achieving the similar rate of weight loss to what other drugs have shown at 12 weeks. Maybe just a last one on CML. I'm sorry if I kind of missed it in the presentation, but just in terms of what the kind of initial pivotal or registration-intended study would be perhaps by line of treatment, I guess, maybe just sort of speak to that and when you sort of can seek engagement with regulators to solidify your initial pivotal plans? Yeah, so I mean, the very fact that we're already enrolling second-line patients in our phase one study and dose escalation through expansion already, I think, puts us in a very good position to go into a seamless sort of registration randomized study in second line. And again, there, the endpoint historically has been six-month MMR. And especially in a scenario where you allow asciminib-treated patients on there, which is already putting your population in a more refractory context than what asciminib did, I think also improves the probability of you getting to an accelerated approval in second line. Obviously, we're still early in the game, but the reason I say that is because there have been historical playbooks that have used similar approaches to get an approval in relapse refractory without taking too much time. Then that sets you up as a pedestal to get to the frontline. And so that's one scenario that you could think of where, given our second-line population already in phase one, that that could transition to a second-line registration program that then could quickly sort of move into the frontline with a study that looked very similar to ASC4FIRST, which is Novartis' frontline study where your control arm is sort of a blend of a first-gen and a second-gen active site TKI. Okay. Okay. So it's basically both hand, right? Over time, it's not one in which you're kind of. Exactly. I said this when we disclosed the data. We don't see any reason why we can't have the same indication profile as asciminib currently has. Right. Right. Okay. All right. Great. Well, let's leave it there for time. Thanks, everybody, for tuning into the session, and thanks, Amy and Emil for the presentation and Q&A. Thank you very much. Thanks so much, Eric. Appreciate it. Thank you.