Good morning, everyone. I'm Sean Laaman, Head of U.S. Mid-Cap Equity Research, Biotech Equity Research here at Morgan Stanley, and welcome to our Global Healthcare Conference. Before we begin, for important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have from BeOne Medicines, CFO Aaron Rosenberg and Head of Strategy John Scotti. Welcome, and thanks for your time, gentlemen. Maybe just to open to a macro question, can you talk broadly about how the company has changed in the past 10 years as it's become a fully integrated global oncology company with capabilities to address industry challenges? That's great. Thanks, Sean, for having us. It's great always to be here at the Morgan Stanley conference. It's hard to go through everything that's changed in the last 10 years. I mean, 10 years ago, the company was nascent. It was a company that had very little revenue, a couple hundred employees, and just really had no significant commercial or manufacturing capabilities to speak of. So much has happened over that 10-year period, with where today we are a leading global oncology company. I think the hallmark of that capability difference is the investment across the value chain in our fully integrated business model from research with our high-throughput research organization through ultimately what we believe is a key differentiating advantage for the company, our wholly-owned global clinical development infrastructure, what we call our global development superhighway. Then pulling that through the remainder of our value chain into manufacturing, into commercial, and behind incredible brands like BRUKINSA, bringing innovative oncology medicines to as many patients around the world as we can. Now our goal is to leverage that incredible capability and do so repeatedly with the cost and time advantages that we've created through that global development superhighway for the next wave of innovation that I'm sure we'll spend a lot of time talking about today. Awesome. Thank you. We're debating this a little bit when we're just chatting just here, but let's get straight into the solid tumor portfolio and before reaching into the heme side of the equation. So you've framed 2026 as a solid tumor inflection point. You got five programs moving forward that are pivotal. To start with, on the CDK4 inhibitor, the BGB-43395, how are you thinking about the registrational strategy and the sequencing across first and later lines? What did the ASCO data change about your conviction in a best-in-class profile versus Pfizer's drug and the established CDK4/6? Yeah, thank you. It's a great question. I think if you step back, it's worth reminding everyone how we developed the molecule and designed the molecule. The molecule was designed to be the most potent against CDK4 in the class and also the most selective. Ultimately, the therapeutic hypothesis behind that was could you hit CDK4 the hardest while also sparing CDK6 and therefore sparing the CDK6-mediated hematologic toxicity that you know impacts many of the real-world dose reductions and dose discontinuations that you see with the CDK4/6 class, including the three that are approved. What we saw in the ASCO data was that that preclinical profile was really translating into the clinic. Just to remind everyone, at ASCO, we showed in the frontline hormone receptor-positive HER2-negative setting, a response rate roughly around 70%, which compares favorably to what you see for the CDK4/6 inhibitors, which is roughly around the low 50s, and a hematologic toxicity profile that is clearly differentiated. So we had, at the recommended phase III dose, zero cases of grade 3 neutropenia, which, to provide some context, if you think about a drug like IBRANCE, the rates of grade 3 neutropenia are in the mid-60% range. Even for the competitive CDK4 molecule from Pfizer, at ESMO last year, they showed rates of grade 3 neutropenia of 26.5%. We think that's a function of our greater selectivity, again, for CDK4 over CDK6. What we also showed at ASCO is how the GI profile can be ameliorated with the co-administration with food. It turns out when you administer the drug with food, you substantially reduce the rate of GI AEs, and it really transforms the GI profile from that perspective. Of course, these are small patient numbers at this stage, but we are in the phase III that is up and running now and enrolling very nicely. We are co-administering the drug with food. Ultimately, this is a frontline trial. The market, as you're aware of in the frontline hormone receptor-positive setting, is quite large. If that profile translates into phase III, it'll be a very commercially relevant profile. GI tolerability that is no different, hopefully, than other agents with a very differentiated heme tox profile that also, by the way, enables combinations with other assets in our own internal pipeline, such as CDK2 degrader, CAT6, and the ultra-potent BCL-2 inhibitor for solid tumor we're developing. All these are in phase I, each of which, or in some cases, has its own intrinsic heme tox. We feel like with our CDK4 inhibitor, we have the ability uniquely to combine with some of these other agents because we do not have a heme tox profile- Heme tox That the other agents have. Sure. Thank you. Maybe ask you about some of the other programs. We can spend a bit of time on your GPC3 x 4-1BB bispecific in liver cancer. John, if you can size the opportunity and your path forward from here on that one. Sure. That's an asset that we're very excited about. I think the reason why we're excited about it, you have to, again, you look at our data we presented at ASCO in an oral presentation. HCC is a very high unmet medical need indication. The five-year survival for HCC is on the order of what you see with pancreatic cancer. There unfortunately has not been a tremendous amount of innovation in this space. What we've developed here is a first-in-class, a GPC3 by 4-1BB bispecific antibody, and 4-1BB is a target that I think many folks are aware of. What's interesting about our 4-1BB is we really feel like we've cracked the code from a scientific perspective on how to engage this axis and do so with a novel binder, novel biology. We really spent some time pre-clinically to design this appropriately, and ultimately, how that's translating into clinical data, we saw roughly in the late-line HCC setting, 30% response rate. For context here, the IMbrave251 trial was presented at ASCO. That's a second-line TKI. The response rate was 5.8%. The response rate in the frontline setting with the standard of care, which is PD-1 nivolumab, is about 30%. So we're seeing response rates in the late-line setting that are roughly comparable to what you see in the frontline setting. We also announced at earnings recently that we fully enrolled a potentially registrational cohort in China in roughly around two months. We plan to start a phase III global trial in the second-line setting by the end of this year, and of course, we're looking beyond the second line and trying to move to the frontline setting as early as possible. From a market size perspective, this market is not small. It's actually a much bigger opportunity than many think. In the U.S., for example, there's about 35,000 patients across all lines. Roughly equivalent incidents to CLL, just for some context. Of course, the difference here is the duration of therapy, and that's the area that we hope to improve upon with this next-generation agent. In Asia, the prevalence of HCC is quite large. There's almost 300,000 patients with HCC in Asia. So it is a very substantial opportunity for us, and it's a first-in-class asset. We're moving as fast as possible. We're excited about it. Thank you. Can you talk about your PRMT5 inhibitor? Can you talk about how that may compare, if it's known, to some of the competitors out there like Tango? Can you talk about the establishment of the relationship with Revolution Medicines and how companies will both benefit from that? Maybe I can touch first on PRMT5, and Aaron, you can transition. I think what we've developed is a molecule that is the most potent against PRMT5 but critically is brain penetrant. We think that's critical differentiation, particularly in lung cancer, where upwards of 30%-40% of patients develop brain metastases. It's a critical unmet need, and it's an area where we believe we will be the only brain-penetrant molecule, assuming all three end up making it to lung, and that's going to be a very important area of competitive differentiation. At ESMO, upcoming, we're going to present the first data set for this molecule. We're looking forward to presenting those data. This is a phase I data set. We're looking at targeted expansions, primarily in lung cancer. Again, we prioritize lung cancer. That's not to say we're not developing into pancreatic and also GBM, which we are. But this will be a primarily lung cancer data set, and we're looking forward to sharing the data. This collaboration is another great example. I talked in the opener just about the power of our global development superhighway. I think the ability to execute and have a transaction with a collaborative partner like RevMed is a great example of the power of that capability. As part of the collaboration, we have the ability, through a clinical supply agreement, to study our innovative medicines with the leading RAS portfolio that RevMed is bringing forth. That includes our PRMT5, that includes our EGFR x MET trispecific antibody, as well as other early-stage programs. As part of the arrangement, we will conduct a clinical trial on behalf, testing our global superhighway and providing that capability for RevMed. In exchange, we will receive commercial rights to the RevMed portfolio for China commercial. Sure. I guess we've spent a bit of time on CDK4, the GPC3 bispecific. When you step back and think about the opportunities on B7H3, B7H4, your PRMT5, and your CEA ADC, which of those opportunities excite you the most? I think collectively, what we're trying to build here is an engine that can generate sustainable innovation over time. What's so meaningful about this wave of five assets is that the CDK4 inhibitor only entered the clinic in December 2023, and it's already moved into the initiation of a phase III trial in just two and a half years. This is wave one, is the point. All of these assets are coming from a pool of substantially more assets that entered the clinic in this timeframe. The way we think about the portfolio is this portfolio will continue to evolve over time, and we anticipate a cadence of solid tumor assets. For example, the assets that are entering the clinic now, we'll see what those look like. Next year, hopefully, we'll have a series of new assets to discuss while these mature in their respective registrational trials. I know I didn't answer your question specifically. Each of them has its own opportunity. I think CEA, right now we're going to be presenting data at ESMO in lung cancer. Obviously, that's a substantial market. PRMT5 could be lung, pancreatic, GBM. These are substantial markets. B7H4, we're looking at studying the agent first in a phase III in ovarian cancer maintenance, and there, the critical differentiation is Not only do you need to have a PFS benefit, but that PFS benefit needs to translate to overall survival. In order to do that, you need to have a favorable safety profile in addition to a favorable efficacy profile, and that's, I think, where we feel we are best positioned. We talked about the PRMT5, and we talked about the GPC3 bispecific antibody. Sure. Thank you, John. A lot of modalities going on, and it almost seems that whatever modality emanates in the oncology field, that BeOne has one. What I am noticing more and more is you are getting this sort of top-line acceleration, but the OpEx does not seem to follow suit. You have got this sort of, I think, some underappreciated earnings compound story going on in the background. How should investors think about that? Thank you. We are very proud of how we have evolved the financial profile of the company. It is easy to forget, but just a couple of years ago, this was a company that was continuing to make investments. It was only last year that we pivoted to generating GAAP profitability, and obviously that is translating this year into increasing leverage, as you said, and most importantly, free cash generation. Candidly, we talked about the profile this year that we are tracking ahead of schedule in terms of both revenue. We updated our guidance on revenue and profit for 2026. We also did provide perspective that with all this opportunity that we talked about with the pipeline, that we will continue to invest. Ultimately, this is exactly where our investors want us to put our capital. We did provide some perspective that continued margin expansion would be modest as we move forward. We provided some perspective on 2027 expenses, as an example, that one might expect 2027 expenses to track at a similar growth rate to what we saw in 2025 and 2026. That was sort of in the mid-teen level. You used your own language about what the profile looks like, but we are investing. We are investing for long-term growth, and we will continue to do so to make sure that we are putting our valuable capital in what drives long-term value. We are not tracking to a specific trajectory of margins. What we are ensuring is that we have sustainability, and we are investing in the potential innovations that will matter for patients down the line. Thank you, Aaron. Getting on to more the sort of here and the now. BRUKINSA putting up its highest new patient starts in more than six years, global sales up 31% in Q2. What is re-accelerating the franchise at this stage, and how do you think about the durability of those growth rates versus a natural maturing curve? Yeah. We spent some time on our last earnings call just talking about the drivers' performance, and we are very pleased with the performance in the United States, but really globally with BRUKINSA. Ultimately, this is driven by the differentiated long-term data that we have shared with BRUKINSA, both in the clinical setting, and then now what we are seeing repeatedly in real-world evidence. And we shared the study of 10,000 Medicare patients, which track both OS advantages as well as duration of treatment advantages for BRUKINSA, which is effectively the translation of that clinical setting into the real world. Growth is really driven by demand. You mentioned that we saw in Q2 our highest level of new patient starts since launch. Behind that is not just CLL performance, but it is the breadth and totality of their five approved indications, which is the broadest label in the class. We do see some advantages on duration of therapy playing out. Again, that is sort of the reality playing forward in our assumptions relative to the real-world experience. All these in total are driving really strong, sustained growth, and we think obviously this will translate to continued durability of the franchise. Awesome. Thank you. Also at Q2, you raised guidance $300 million, operating income by $250 million. What is really driving your conviction in raising those performance metrics? It is what we are seeing in the marketplace. We talked about the strength of our U.S. franchise with BRUKINSA. We see it globally, really strong performance with our European business, where we are a bit earlier in the launch trajectory, even earlier when you think about rest-of-world markets, important markets like Japan and Brazil. Ultimately, our conviction is driven by the differentiation of BRUKINSA and how that is translating to demand. And ultimately, that led us to increase our guide by $300 million, as you said, on the top line, and that translates to bottom-line performance while we continue to still invest for growth for the long term. Sure. Just thinking, moving towards where we are in the back half of the decade, just underwriting the growth in BRUKINSA for the back half of the decade, and what underwrites that? Well, I think there's still plenty of opportunity. We're not satisfied with the share that we're capturing today. We have plenty of opportunity. We're obviously the leader from a value perspective, but even from a new patient starts, there's more opportunity to ensure that BRUKINSA is prescribed in the marketplace for the patients where it continues to be, in our view, the best BTKI based on the totality of the evidence. We do have new indications that we believe will drive increased growth. We talked about the MANGROVE data, which is in the frontline MCL setting, the first chemo-free BTKI, which really provided from a hazard ratio perspective of 0.57, the best outcomes we've seen in a clinical trial in a frontline setting. MCL is not as large as CLL. It's still about one-fifth that opportunity. Importantly, MCL is a space where BTKIs are relatively under-penetrated. So this is an area with a chemo-free regimen to really make a difference for patients and to drive growth for BRUKINSA. We have other studies which potentially read out in the years to come, including MAHOGANY, which is in the MCL follicular setting, and then ultimately our broader hematology franchise in the combination with BEQALZI, and then ultimately with tacabrutideg, our degrader, really to satisfy patient need across the continuum from the frontline setting through the late-line setting in CLL and beyond with their approved indications. Sure. Looking at ex U.S., where is Europe and the rest of the world in its trajectory, and is that the most underappreciated piece of the commercial story today? Well, I think there's a lot that we'd love to see more appreciation for, but obviously. Our European business and our rest-of-world business, particularly big markets that I touched on, they're just a bit earlier. They continue to perform very well. Similar to the U.S., they're tracking well in terms of their new patient start capture. But there's still more opportunity as the franchise continues to grow and evolve. Overall, I think we feel really confident in where we sit, but there's more opportunity to go in that setting. Awesome. Changing gears a little bit, so on policy tariffs and corporate structure. Let's talk about the agreement you announced with the U.S. government recently. You're joining a federal pricing framework which would price future FDA-approved products in line with other developed markets. Can you share more details on this, and how should we think about the impact of most-favored nation-style pricing on either your current or future launches? Sure. Like many of our peer companies, we've voluntarily agreed to participate in the GENEROUS model. This is with respect to TEVIMBRA, our PD-1 inhibitor, which provides access to MFN-like pricing in the Medicaid setting for TEVIMBRA. BRUKINSA and BEQALZI are not in scope for that agreement. Additionally, we agreed to price future launches outside of those products with pricing consistent with those found in developed markets around the world. We also committed to an onshoring agreement consistent with our broader supply chain strategy to bring U.S. manufacturing to support U.S. patients. We've invested $800 million in our Hopewell facility, which was very biologics focused. We recently announced a $300 million investment for drug product manufacturing and small molecules. This is just, from a totality perspective, our continued investment in our global infrastructure for access, including the support patients in the United States. Wonderful. Thank you. You just mentioned TEVIMBRA. We've seen the recent approval of Ziihera in GEA. How do we think about that as a tailwind for TISLE? Yeah. It is certainly a very nice incremental opportunity as we continue to globalize TEVIMBRA. We have been in the process of launching in Europe and the U.S. and in markets outside. This is a great tailwind for that franchise. Obviously, the data with the HERIZON-GEA-01 data is differentiating. We are talking about seven months of OS advantage. We do believe that the triplet will be practice-changing. It is obviously very early days in terms of the launch trajectory there. But we think this is a sizable opportunity. There is, I think, using the data that Jazz Pharmaceuticals has disclosed, about 8,000 patients in this setting. So we do believe that this is a great opportunity for TEVIMBRA in the U.S. and other markets in which it launches to continue to support the globalization of the brand. Right. I guess you are the only company with foundational therapy in all modalities around B-cell malignancy, so the BCL-2 inhibitor, the TKI inhibitor, and the degrader. What is the rationale behind owning all three? I think the clear rationale is to be able to combine these agents in ways that can drive patient benefit and value for patients and that other companies are unable to access because they simply do not have access to these three foundational medicines. I think Aaron touched on it earlier. The overarching goal here when you think about how we are developing this franchise is to have a BeOne regimen as the best regimen for patients, driving the greatest long-term benefit for patients, regardless of line of therapy or treatment preference. So we have BRUKINSA as, in our view, the best-in-class BTK inhibitor. We will talk about perhaps ZS in the fixed duration space. That is currently in two phase III trials. Then we will also be working on and potentially talk about the degrader in the relapsed refractory setting. Sure. On that sonrotoclax and BRUKINSA combo, just remind us what the next signposts are, and do you think the street adequately appreciates the revenue opportunity from that combo? With regard to next signposts, this is in two phase III trials. The regulatory endpoint for both of those trials is PFS, and these are event-driven endpoints. The first trial is a head-to-head versus venetoclax plus obinutuzumab, which is the current standard of care for fixed duration in the U.S. It is about 20%; 25% of patients receive this regimen. There, we are looking to improve upon some of the issues we see with venetoclax obinutuzumab. As we talked about in earnings, this is a regimen that at six years in all comers, if you just look across trial, of course, the six-year PFS is roughly 20% below what we see with continuous BRUKINSA. In high-risk patients, which is more than half the patients, it is 28% below. You have to deal with the limitations of obinutuzumab infusions. You have to deal with the ramp-up of venetoclax and the lack of feasibility to be able to expand that into the community setting. Also from the safety side, the CLL 17 trial taught us that even after you stop therapy with VO, you still see elevated rates of serious infections for up to three years after stopping treatment, which is higher than continuous ibrutinib, which was the comparator in that trial. Continuous ibrutinib never catches up. The reason for that is because obinutuzumab, it is a blunt weapon here. It completely obliterates the entire B-cell repertoire, and that prolonged depletion of the immune system lasts well beyond the fixed one year of treatment. Despite all that, when you look at these trials, CLL 14, 17, et cetera, half the patients who progressed on that regimen actually, unfortunately, died. Naturally precludes the opportunity to retreat these patients. What we are trying to do with ZS is develop a regimen that patients who opt for a fixed-duration regimen will not have to sacrifice long-term outcomes relative to what they are able to achieve with a well-studied continuous BRUKINSA, which is very convenient in a daily pill that can be taken for a long time. I think the other option here is acalabrutinib plus venetoclax, which was recently approved in the U.S. We have a separate phase III trial that is head-to-head of zanubrutinib plus sonrotoclax versus acalabrutinib plus venetoclax. That trial is slightly behind simply because ABBV-101 was not on the market yet. It is slightly behind the head-to-head versus VO. There, based on the AMPLIFY data, which in that trial they enrolled a patient population that was roughly 10 years below the median age of diagnosis of CLL and excluded high-risk patients. Despite that, saw the lowest rate of three-year PFS of any of the major regimens and the lowest rate of undetectable MRD that was actually worse statistically than chemotherapy. We feel like that is a lower bar from that perspective for us. We want to unambiguously demonstrate, hopefully pending the phase III results from that trial, that we have a better BTK and BCL-2 combination. Sure. On competition, are you seeing any impact from acalabrutinib with any combo on your business? It is still early days. Europe has historically been a bit mature in this space because ibrutinib plus venetoclax has historically been approved. We see a bit more traction in the European market. It is just a market that is more primed for BCL-2 and BTKI combination. The U.S., it is still early days. The approval was in February. We have not seen meaningful traction of yet. But we continue to be mindful of competition and are doing our part to ensure that the BRUKINSA data continues to be out and appreciated in the public domain. Sure. Similar question on pirtobrutinib, just to get your latest thoughts on that as a potential 1L entrant in CLL. Yeah, it is a great question. I think it is important for pirtobrutinib also to recognize how the drug was designed and developed. This was an agent that was designed specifically to retain activity against patients who develop C481S mutations, which would otherwise abrogate activity to the covalent inhibitors. It does that really well, and it is approved in that setting. It benefits a lot of patients in that setting. But the question was, what does the data look like in BTK-naive patients? We got the answer to that question last Ash, where, for example, we saw data from the BRUIN-CLL-314 trial, which was their head-to-head trial against ibrutinib. In that trial, two-thirds of the population was relapse refractory. In the SAP, that is the key secondary endpoint that they will need to hit to be able to show superiority to ibrutinib. Those results were underwhelming. I think the hazard ratio was 0.845. The P value was 0.4. If you look at the IRC data, there was only two events separating pirtobrutinib from ibrutinib in that trial. It was 48 versus 50. If you compare that to what we saw with zanubrutinib versus ibrutinib in ALPINE, we saw a hazard ratio of 0.69, so a 31% reduction in the risk of progression that was statistically significant, with a P value of 0.01. Early separation that was sustained, and we also have much longer-term follow-up data. I think the point I am trying to make is we think we're going to be the only agent that can say we have demonstrated PFS superiority against ibrutinib in a head-to-head trial. The other piece on pirtobrutinib, too, is the safety. And in that head-to-head trial, the safety was perhaps more surprising because the safety was actually, in many cases, numerically worse than ibrutinib. It was better than ibrutinib in AFib, but the AFib rates were roughly comparable to what we see, again, across trial in SEQUOIA. So you have to ask the question: for pirtobrutinib to be used in the front line, it needs to generate outcomes that are above and beyond what have already been shown with zanubrutinib. Also because in order to make that decision, you have to give up the opportunity to use pirtobrutinib in the later line setting, where it is already benefiting patients in a way that zanubrutinib is unable to do because we're not a non-covalent inhibitor. We don't have activity against those C481S mutations. And the conclusion really to us when we look at the data is there's no need to change the treatment paradigm, and the treatment paradigm and the data support BRUKINSA as the best-in-class first-line therapy. Sure. Going back a little bit, but following the zanubrutinib and sonrotoclax combo and the CERTI-031, the uMRD update that you provided, how should we think about the uMRD data and the read-throughs to the PFS endpoint? Thanks for asking. That's an important question. For everyone's awareness, we did announce at our earnings call that we did not reach the statistical superiority for undetectable MRD in that trial. Importantly, a couple of things. One, this was a very high scientific bar, and I'll go through why that was the case in a second. But it doesn't change two things. Number one is the regulatory strategy and timelines, and number two is our confidence in the ultimate regulatory endpoint here, which is, as we mentioned earlier, PFS. So on number one, uMRD is not an accepted regulatory surrogate endpoint for approval, as it is in myeloma, and PFS is the clear regulatory endpoint. Sure. On number two, it is important to consider that the MRD rates in CLL are actually dependent on the types of regimens that you use to combine. So in other words, venetoclax and obinutuzumab had an MRD rate of 73% in the CLL17 trial. Ibrutinib plus venetoclax, which was compared head-to-head versus VO in that same trial, had an MRD rate of 46%. But remarkably, the Kaplan-Meier curves were superimposable. This is because it seems to be that there is a mechanism dependence with regard to MRD. What we have shown in our phase I results is the highest rates of uMRD for a BTK plus BCL-2 combination of north of 90%. Again, this compares to IV in the mid-40s in CLL17 and AV, which is even lower than that, in the roughly 30s range in the AMPLIFY trial. That has translated, hopefully we will see, into a PFS benefit. That is ultimately where our confidence lies in the PFS endpoint. Sure. Thank you, John. On to the degrader, I just want to make sure we talk about that. It is heading toward a potential accelerated approval submission into 2H26, and you are studying head-to-head against pirtobrutinib. How are you thinking about potential market opportunity here and the competitive positioning? Sure. So with respect to the guidance, we have guided to provide an update on a potential accelerated approval filing second half of this year. We will have more to say when we have something to say. I think you also referenced the head-to-head trial that is currently ongoing and hopefully will finish enrollment in early 2027 versus pirtobrutinib. Our confidence in that trial is twofold. First, it's mechanistic. This is an interesting mechanism because it is able to retain activity against a substantial number of mutations in BTK that would otherwise render pirtobrutinib inactive. It's important also to remember that pirtobrutinib, it's an ATP-competitive inhibitor that binds to the active site. Which means if there's a kinase dead mutation, if there are other active site mutations, it no longer works, right? No different from the covalent inhibitors. What the degrader does is it targets the whole protein for proteasomal degradation, which means it retains activity against those mutations which would otherwise render pirtobrutinib ineffective. It also retains activity critically against the scaffold function of the protein, and where the kinase activity does not signal and yet or there's no signaling from the kinase activity, but you still see BTK pathway. There's a mechanistic reason here, and then ultimately there's the clinical data that we've generated. The clinical data so far, it's cross-trial comparisons, of course, but we've shown a mid-80s response rate in fifth-line CLL patients who really don't have many other options. The vast majority of which, upwards of 80%, had seen BTK and BCL-2. At the recommended phase II dose of 200 milligrams, that response rate was 94%. Our median PFS in the most recent update was two years. That compares to what pirtobrutinib saw in the BRUIN CLL-321 trial in roughly the same setting. Slightly less pretreated, one line less therapy, roughly half of patients had seen BCL-2, so less pretreated from that perspective, and their median PFS was roughly a year. If that translates into a phase III, the goal here is to unambiguously show in a head-to-head trial that tacabrutideg is the better option for patients in this setting. With respect to the market opportunity, I think we could look at what pirtobrutinib is annualizing at right now, which is nearly $800 million, and it's approved in that setting, and it's growing quite nicely. So I think there is a real market here and- Sure. That's the opportunity that we have ahead of us. Well, we're right at time. We've touched on a lot. We've touched on the strategy, the financials, solid tumor portfolio, the outlook near-term for BRUKINSA, what you've got in various combos, and other things on the heme side. Is there anything that I didn't ask before we sign off? No, I think we covered a lot of ground. We really appreciate your time and questions. We're really excited about how the current year is performing and all that lies ahead. You asked about what reflecting back 10 years ago to where we are today, what we're really focused on is what we're going to be 10 years from now, and we're so much opportunity in front of us. Awesome. Well, thank you, gentlemen, for your time. It's wonderful. Thank you. Thank you so much.