Potential synergy that you can get when using zanidatamab, a highly immune-active antibody, in conjunction with immune checkpoint inhibitor like tislelizumab. Really pleased with that, and on the heels of it, remember we had stat sig overall survival benefit for the triplet arm at the time of the first interim analysis with two additional scheduled OS analyses. At that time, the arm B or the doublet arm was trending very favorably but not quite stat sig. On the second interim analysis, we now have a stat sig result for the zani-chemo versus the control arm. Encouragingly, as we said in our press release, the hazard ratios for both of the experimental arms continue to improve even from the first interim analysis when you look at the overall survival, which is consistent with highly immune-active drugs, where you tend to see that benefit beyond the medians. Later on that curve, you see more durable benefit, and you would expect to see the curve separate. We are excited to publish those data as soon as we can at an upcoming medical conference. Just quickly mention some other areas that we are leaning into on Ziihera. We have our frontline BTC trial, which is well underway. We have our late line. That is pivotal trial. We have our late line breast cancer pivotal trial that is well underway. We also have a pan-tumor trial that could get us a tumor-agnostic indication, meaning any patient whose tumor overexpresses HER2 and is refractory to standard therapies could potentially get it. Within that trial, we have had some interesting colorectal cancer results. That combined with other data we had earned us breakthrough designation with the FDA, and we are working with them to plan on an approval path in colorectal cancer while we pursue broader indications, potentially even including non-small cell lung cancer. Clearly, Ziihera has made a lot of progress. We think its unique mechanism of action is highly differentiated and is really best in class, going to be a new standard of care in biliary tract and gastric cancer. We are investing heavily behind that, as I mentioned, in our pivotal trials. Super excited about our epilepsy portfolio as well. We announced recently that EPIDIOLEX, which has a very long period of exclusivity into the late 2030s. We are initiating four new clinical trials, as well as having submitted an application for a solid oral dose or capsule formulation. Those new trials include a phase II in focal onset seizure as a kind of evidence generation trial. It includes a phase II/III potentially pivotal trial in juvenile myoclonic epilepsy. It includes a phase III in a broad array of DEEs. Of course, we have an indication for seizures associated with three orphan DEEs, so this potentially will broaden that label even further. We have an evidence generation study in LGS in adults to further support the use in that setting. Super excited about EPIDIOLEX and its impact it is having and the longevity there. We certainly think of ourselves as an epilepsy company. We have mentioned in the past, we have two pipeline products, one for absence epilepsy in phase I, and we have now recently plan to bring our Kv7 into phase I, which we think is potentially a best-in-class Kv7 opener. In addition to that, very pleased to say that yesterday we closed on the Actio deal. You haven't seen the data on that yet. I mean, we certainly have as part of the due diligence, and we hope those data will be published soon. We were very excited to be in another rare epilepsy where, in this case, we think this inhibitor addresses specifically a single gene mutation, which is responsible not only for the epilepsy in these patients but the developmental challenges that they experience. A targeted, personalized medicine here could make a tremendous difference based on the pre-clinical and clinical data that we've seen. Also excited that the ACTION trial for Modeyso continues to progress as planned, and we've reiterated the timing next year on the interim analysis for overall survival that would give us an early opportunity for approval in frontline high-grade glioma. Currently, our approval is in refractory high-grade glioma. That's an interim analysis, so if it doesn't hit, the trial continues until completion. Lastly, just recently announced that our next generation orexin two agonist has cleared the IND and is expected to go into healthy volunteer studies this year. That's kind of the key highlights from my perspective. Maybe I'll pause there and leave it open to any questions you might have. Great. Thanks, Rob, for that intro. Maybe if we could unpack a little bit of the history on Ziihera on Zani. Could you remind us what got you interested initially in doing the deal with Zymeworks to bring in the asset? Maybe you could also speak a little bit to the HER2 mechanism and its differentiation- Sure. within the class and how that might, for instance, impact what we're seeing in both the PD-L1 positive as well as negative patients. Yeah, thanks. Great question. We were interested in zanidatamab, I would say in the earliest stages because of the novel mechanism of action. This is the first HER2 antibody that had a biparatopic engineering structure. What that means is that each antibody actually has specificity for two different binding epitopes on the receptor. Now, those binding epitopes were selected because they were clinically validated. It is ectodomain four and two. Those correspond to where Herceptin and PERJETA would bind. What differentiates it is when you put it on the same antibody, each Fab fragment of the antibody has to bind different receptors, unlike giving Herceptin and PERJETA together. When that happens, the antibody binds to one receptor. The other Fab fragment can't reach that binding epitope on the same receptor, so it grabs a different receptor and pulls it in, and then sequentially happens with the additional antibodies. What that does is cause, and this was demonstrated in the Nature Communications paper, it causes receptor capping and clustering, internalization, but also importantly, fixation of complement. What really differentiates this molecule is it triggers the complement cascade, and that does not happen with any other antibody. It was also engineered to have a highly active Fc fragment. If you think of the antibody as a Y, the Fc fragment is what typically induces immune responses, recruiting macrophages and NK cells. You have complement cascade activation, you have recruitment of NK cells and macrophages. You have an antibody that not only blocks HER2 and HER3 signaling internalization of the receptor, but triggers the immune system in a way that other antibodies don't. It is for that reason that we had the hypothesis that this could synergize with PD-1 inhibitors. When people were surprised that we had activity in the frontline gastric trial in the PD-L1 negatives, and I could see why that would be a surprising result, because four prior studies with three different PD-1 antibodies all showed no activity in PD-L1 low patients, including the KEYTRUDA trial in HER2 positive disease and including tislelizumab in the all-comers population. Yet our phase II showed we had activity in PD-L1 negative patients, and we think it is because of the immune activation that happens with zanidatamab. That mechanism of action is what really first got us interested. It was early days, though, and we hadn't seen much clinical data, so our business development group made a $50 million bet to say, "We get an option once the biliary tract data come out, and if we don't like it, we walk away, and we give up the $50 million." We were very pleased with the biliary tract cancer data. As you know, over 40% response rate, very durable. If you look at the IHC 3+ population, which is what is in the label, response rate. That really is very differentiated from any historical data with Herceptin and PERJETA, which never achieved approval in that setting. We also thought they had very logical development paths, so fast to market in biliary tract, going after some clear white space where it could win in frontline gastric cancer, where only Herceptin was approved. Then we felt the deal paid for itself on the basis of those two indications. But we also saw in the phase I data and based on the mechanism, the opportunity to go much further beyond that, as I described earlier. Great. I know you've articulated a little bit about your thoughts on the label that you received for Ziihera, but as we think about how docs will employ the product in practice, you have a triplet as well as a doublet regimen. How do you think the physicians will start to utilize those regimens? The doublet I noted is restricted to IHC 3+ patients. Yeah. Is that in any way a limitation? I'll address that first, and then I'll talk about what I think is the best use for this drug. I think it's not really a meaningful limitation. First of all, it's a very small proportion of patients from an epidemiologic perspective. In the trial, it was less than 20%. But I also think it's clear from the data that in that small subgroup, that the trial wasn't designed to address, there's clearly confounding factors that explain it. For example, if you look in the label, you can see that the trastuzumab control arm was wonky. What do I mean by that? The IHC 2+ did better on tras-chemo than the 3+, which is not only biologically implausible, but it's never been seen before. It's always been the case that Herceptin does better in 3+ than 2+. It tells you that small proportion of patients is not behaving the way you would think. When we look patient by patient, because it is a small group, you can see that their baseline characteristics were not balanced. We think that is not a meaningful result. We do not think it will impact practice anyhow. We certainly had that discussion with FDA. They tend to follow the data, and we will see. Maybe with additional updates, we could revisit that. In any case, I do not think it is meaningful, and I do not think it will impact practice. To your first question, which I think is the more important one, what has happened here is we are a little bit maybe the victim of our own success. zani-chemo looks so good that now we get the question, well, could you just use zani-chemo and not add sacituzumab? For me, absolutely the answer is to use the triplet for a number of different reasons. One is that the triplet data are stronger in our trial. Clearly, it is adding. You cannot look at just the medians for OS. You have to look at the whole hazard, and you will see when we put the update out, it persists. You get this flattening of the curve. Interestingly, with both the triplet and the double, it becomes pretty flat. That is why you are seeing an improvement in the hazard ratios over time. At those later time points is when you really start to see some differentiation. You see that added benefit of a PD-1 inhibitor, which is highly consistent with all the results previously. There have been now five trials of PD-1 inhibitors in frontline gastric cancer and another in early-stage gastric cancer where PD-1s have a survival benefit. We know that immune therapies are the potential curative therapy. The idea, I talked about the synergy potentially between zanidatamab and a PD-1. If you are a patient with, by the way, still a very poor prognosis disease, where the risk of death is high at 5 years, you want to give all your therapies up front, and you want to potentially take advantage of that synergy between zanidatamab and a PD-1. I think unless there is a contraindication to a PD-1 inhibitor, which is relatively rare, patients should get that. There are some additional toxicity, but it is easy to distinguish what is coming from where based on timing and the nature of the toxicities, and it is manageable in the right hands. I do think that the right approach is to use the triplet irrespective of PD-L1 status and then IHC 2+ or 3+. That will certainly be the focus of our marketing and our education. I want to get into the commercial dynamics a little bit of the Ziihera GEA launch. I think you have talked about 8,000 HER2-positive patients, the populations that came out there. You've also talked about, I think, a 3,000-4,000 number as perhaps the Ziihera treatable population. Can you help us understand what costs you employed to get to the 3,000-4,000 addressable patients? Is there any consideration, for example, for potential competition, let's say, from ADC? I'm thinking, for example, of the DESTINY-Gastric05 trial winners. Yeah, maybe I can jump in there, David. Thanks for the question. When we think about that 8,000 patient population, that's really an incidence of HER2-positive GEA. When we think commercially, that 3,000-4,000 treatable patients, that's really taking into account unresectable disease, treatment in the first line, and testing rates. So it's a true treatable population, and we do think, to Rob's point, we do have a differentiated asset here. We did just launch three weeks ago. I know Chumi and Sam and team are. They were out there on the first day, and I think we're all quite excited to get that on the market. When we look forward, and we think about competition, I do want to be very clear. We do expect to be the standard of care. We're the only regimen that's being actively promoted in the first line. We do think zanidatamab should replace trastuzumab in every patient in first-line GEA. To Rob's point, we think most patients should be treated with a triplet in combination with tislelizumab. When we look to the future, there are some first-line trials. David, you mentioned T-DXd here in HER2. Those don't read out until 2029, and frankly, we've set a very high efficacy bar to which they will need to beat. The data we've seen to date has been phase II data, and I think our data certainly speak for themselves when we look at the marketplace in the future. I would just add both on the addressable population and the future competition. We do see opportunities to grow this market. One thing that's personally frustrating to me as a practicing oncologist is that the utilization rate in frontline GEA of HER2 drugs in general is lower than you'd expect. I mean, for me, it should be 100%, even before the zani datamab, but especially with the zani data. It hasn't been. For one reason or another, even though testing rates are high, not everyone's benefiting from HER2 therapies. Could that be because maybe the benefit wasn't as significant as we now know it is with zanidatamab? We are certainly going to get out there and educate around, your patient who has HER2-positive disease, as defined in the trial, should get Ziihera and is going to benefit from it, not only directly but through the synergy with the PD-1, and hopefully increase those treatment rates. I think there is an opportunity to grow that market a bit. Then with regard to the competition, ultimately, we will have to see the data, and I think the data will win the day. To Jack's point, Ziihera has a head start, and it has very strong data. The other thing I would point out is that frontline chemotherapy, whether it is FOLFOX or CAPOX or metastatic GEA, is quite good, and the practice here has been to use a targeted therapy and a PD-1 inhibitor on top of that backbone chemo and to give the chemo for a period of time. There is probably some interaction there. We learned over the years that giving some chemo there, especially the right kind of chemo, can help synergize with PD-1 inhibitors. That is generally the practice is to give some chemotherapy for a period of time, and then as patients begin not to tolerate it, you can modify the dose. You can drop it entirely. You can stop it. Then the paradigm really is continue the HER2, in this case, zanidatamab, continue the PD-1. These are the drugs that drive long-term survival. When you use an ADC, you do not have that opportunity. We are talking about gastric cancer. It is true for frontline breast cancer as well. You give an ADC, you are stuck with the chemotherapy for this. You cannot drop the chemotherapy component. We think the treatment paradigm is pretty well entrenched, and the flexibility that you get from zanidatamab, which is highly immune-active, yet not an ADC, does not carry that toxic payload, is a real advantage there. We are also thinking about that in the breast cancer context, where really the paradigm, even in frontline breast cancer, has been to drop chemotherapy over time and continue the HER2 agent, which I hear more and more talk about that for an HER2 induction within HER2 and then move to a maintenance non-ADC HER2 agent. Investors are certainly looking forward to seeing the GEA launch play out. We will definitely keep tabs on that. I want to spend some time on the next chapter for zani, and that is in breast cancer. I believe coming late 2027 or early 2028, we should see results from the phase III IMpower03 trial in post HER2 metastatic breast cancer. As we now approach this next key readout, how should we think about the probability of success here for this study? Keeping in mind that this is a later-line population that has previously been exposed to prior HER2 therapies, how should we think about the performance of the zani arm versus the comparator arm, which is Herceptin and chemo? Yeah, thanks for that question. I loved your first question because it took me back three-plus years, where it's sort of like, what did you see there that others didn't see? As we started to get data, I've asked myself, what are we learning from these data? As a principle, what we've learned is that wherever HER2 is the backbone or wherever there's cancers that overexpress HER2 but don't get Herceptin as a backbone, zanidatamab is going to compete very well. The other principle is when you can combine with a PD-1 inhibitor, that's going to do well. I'll come back to other settings where we think we have an opportunity to do that. What's relevant to your current question is, why do we think this trial is likely to succeed? Well, this is another opportunity to go head-to-head with Herceptin in the design of the trial. Now, we acknowledge that this is a later-line trial. It was, to me, the obvious first place to go, and it's certainly, I would say, very consistent advice we got from all of our breast cancer experts to say, in a world where patients getting HER2 upfront, at least upfront or in second line, it's unclear what to give then as a HER2 agent. Every one of these breast cancer patients will continue to get HER2 therapy, even as their subsequent line chemotherapy changes. So it was the obvious first place to go, and we think that our chances are good because, again, we're head-to-head against Herceptin. It gets our foot in the door in breast cancer. We revised our projections on what we think the potential is for Ziihera. By no means is that the only area of breast cancer that we're interested in. So we are planning to get into earlier lines of breast cancer, and we think our path to do that will be in combination with a novel HER2 TKI. So why is that? Well, we know when you're combining with the TKI, there's some synergy there, because TKIs tend to at least stabilize HER2 on the cell surface. They sometimes cause upregulation of TKIs, and that really plays right into zani's mechanism of action, where when you have a lot of HER2 on the surface, it clusters, triggers the complement cascade. So we think that combination makes a lot of sense. We're now seeing next-generation TKIs that are much safer and more effective because you can go to higher exposures because they're more targeted. They don't hit EGFR, for example. We have a collaboration with Boehringer Ingelheim on zongertinib, that's ongoing in breast cancer. We also partner with Iambic on their IAM1363, and both of those have the potential to be best-in-class TKIs. So we think that through a combination with a novel TKI, we can move not only up in line in breast cancer, but we could also potentially get into more difficult-to-treat populations such as brain mets. We're also interested in early-stage breast cancer because zanidatamab as a monotherapy is so well-tolerated. We talked about the advantage of not being linked to a chemotherapy payload that in some cases causes fatal pneumonitis, as in the case of ENHERTU. You can then use that as a de-escalation strategy in highly curative settings. So that's the whole goal of the I-SPY collaboration is can you use zani up front as a more effective therapy and minimize ultimately the amount of chemotherapy that a patient gets, which would be a super advantage. It also has the flexibility then to be used in other settings. So we've got the I-SPY collaboration, we've got an MD Anderson collaboration, and we've got a phase II of our own in that pre-surgical or so-called neoadjuvant and adjuvant breast cancer setting. We'll look at those data and decide what our best path forward is in terms of a registration trial there. So very excited about breast cancer. We're really pleased that we took that step of starting the breast cancer trial when we did, even before we saw the gastric data. I think opportunities to lean in there as well. Great. Well, so to recap here, you've given previous guidance of $2 billion-plus, I believe, for Ziihera. Now thinking about building towards a $3 billion to $5 billion number with some of these additional indications you talked about. Maybe to wrap up here with Ziihera, could you just tell us a little bit about your efforts with the pan-HER2 label, a tumor-agnostic label, and how important is that potential label for building towards your potential peak sales number? Yes, it's a great opportunity, we think, because everywhere we've tested Ziihera in patients who have overexpression, regardless of their tumor type, it works, and it seems to work better than prior agents. So we think we can generate the data in our so-called basket trial or pan-tumor trial that would give us a tumor-agnostic indication, and we're enrolling that trial, and we're well on the way. In that trial, interestingly, we are enrolling some populations that are less rare. We got the really rare salivary gland tumors, for example, and other rare tumors. We also have some colorectal cancer patients coming on, some non-small cell lung cancer patients coming on. What we saw, we haven't published these data yet, but we're seeing activity there in colorectal cancer. That in addition to what we saw in colorectal cancer in the phase I, and in addition to the dedicated trial we did in frontline colorectal cancer with backbone chemotherapy, altogether, it looks like we've got some significant activity in colorectal cancer. We brought that to the FDA. We received breakthrough designation for second-line colorectal cancer. We're in discussions with the FDA on the path to a rapid approval in colorectal cancer. We don't have as much data in lung cancer, non-small cell lung cancer, but that's an interesting space as well because the HER2 approvals in non-small cell lung cancer have been around activating mutations. They haven't been around overexpression. But we think the epidemiology is such that overexpression is less common there, and there there's no approved HER2 therapy. So this pan-tumor trial is not only potentially going to get us a tumor-agnostic indication, it will give us some data we need to perhaps set a path toward an approval in colorectal cancer, maybe even down the road further, non-small cell lung cancer. Then maybe, since I know you want to wrap up on Ziihera, I will just mention a couple other things. We talked about the principles of wherever you can go head-to-head, either with Herceptin or nothing in a HER2-driven tumor or combined with a PD-1 inhibitor, where would you go? That is the situation with frontline BTC, which is an ongoing pivotal trial that is already enrolling no approved HER2 therapy. So it is against nothing. We know we are highly active in BTC. Most patients, I think probably 80% of the patients globally, will be getting a PD-L1 inhibitor or a PD-1 inhibitor in combination. So we are very optimistic about that trial and looking to enroll and bring that in. I am super excited about it because other biomarker-driven trials in that setting have failed. If you look at the FGFR experience, I think they screened 5,000 patients and never enrolled. We now know that this trial is going to be successful to enroll on the timelines that we are planning for, and I think that is first, which speaks to Jazz's ability to execute in rare disease spaces. Then lastly, we have not made a commitment yet in gastric cancer. But again, to illustrate those principles, we have highly active in gastric cancer, HER2-driven disease where there are no HER2 approved therapies in the resectable space, the early stage resectable gastric cancer, and IMFINZI is approved there. So we are deep into planning on can we do early stage neoadjuvant, adjuvant gastric cancer study as well. I think overall, that illustrates what we are thinking about when we revise the potential into that $3 billion-$5 billion range. Great. I would be remiss if I did not spend some time on the rest of the programs and pipelines because you have so much going on. Maybe this is a good time, a good segue to pivot to sleep-wake. So here, I think two straightforward questions. We know that this is an evolving space with multi-source generics, oxybates, things like that. So how are you thinking about the durability of the Xywav franchise looking forward? Then given so much of the activity around orexin, how important is having an orexin molecule of your own to remaining competitive in the space? Yeah. Of course, I am the R&D guy, so what I say on the first question, take it in that context. For me, Xywav is not Xyrem or LUMRYZ. It is highly differentiated because of the low sodium, the lack of sodium there that for the other formulations really causes a meaningful cardiovascular risk. Prior to generics on Xyrem or prior to the LUMRYZ, we really entrenched ourselves and I think educated well physicians on the importance of low sodium and published data showing that if you use a high sodium oxybate, patients develop hypertension in pretty short order. I think people understand that benefit. They also understand that Xywav, because of its optionality of giving it twice a night and giving it in different split doses, the flexibility that comes with that and the added efficacy that you get by using a second dose is differentiated from LUMRYZ and that a once-nightly formulation really is not the advance people might have thought. I know less about payer dynamics as the R&D guy, but I think what we are seeing is durability of Xywav through some of that competition and through the Xyrem generics. In terms of what we are learning about the orexin space, we have been pretty consistent from the beginning, and I think it is interesting to see that now the data are coming out, that the field is coming around to our position on this. We have said that hypersomnia is narcolepsy type 1, type 2, idiopathic hypersomnia are at its root cause, a disease of disrupted nighttime sleep and all the symptoms of sleepiness during the day and cataplexy come from that. While the mechanism around orexin is interesting and is somewhat directly related to the underlying pathology, at least in the NT1 population, giving an orexin 2 agonist is not the same as repairing the damage to the orexin neurons that happen through autoimmunity. You do not recapitulate the orexin system. You simply hit that target, and it causes wakefulness. What is the evidence of that? When you give an orexin agonist during the day, which we hypothesized, and we now feel it is proven, even though all the data are not out there, you do not fix nighttime sleep. If you look at the PSG data out there, everyone who has done the PSG, the only discussion about the potential benefits of nighttime PSG is around REM, which is not surprising at all because if you give a stimulant, then you avoid some of the symptoms that narcolepsy patients get when they go too quickly into REM. But it does not address the root cause of sleep disturbance, which is not getting enough sleep, total sleep time, and not getting enough deep sleep, which is called N3 sleep. In fact, especially when they are longer half-lives, orexins are probably disrupting that further. If they were improving nighttime sleep, we would have seen all the PSG data that companies already have, and we do not see it. And we will evaluate that with our own for sure, because we think ultimately orexins are a very good daytime wake-promoting agent and could be complementary to Xywav, but we don't think it's going to replace it. The second part of that question, David, is just a little bit more on the field. The approvals in NT1, which requires a much lower dose. What happens is when you get loss of orexin neurons, the receptor levels for orexin go up, and then you need much less drug to hit those receptors. There's not an approval yet in other hypersomnias. And that approval is with a drug that has a very long half-life, and the other ones in development also have a long half-life. I think there's an opportunity to optimize, have a drug that's very good brain penetrance, so you don't get systemic toxicity, has a much shorter half-life that can either be used as is or formulated in a way that you get enough coverage during the day. Because we're hearing loss of effect at night, onset of cataplexy in the morning. You get enough of an effect that you don't have the carryover of insomnia. So we will see. It's early days. We just cleared our INDs. We announced our program's goal to have a shorter half-life drug, that's something that's differentiated, also in terms of other features like brain penetrance. And this is a mechanism that you could test pretty well in healthy volunteers, and so we expect to have some data in the near future. We could spend just a minute or so on the epilepsy franchise. So EPIDIOLEX, obviously a very successful product since you did the GW acquisition. We're continuing to see nice growth and a long IP now on that molecule. Could you talk us through a little bit about the clinical development plans for EPIDIOLEX here? I know you have some potential additional follow-on indications and how do you see those growing the product beyond its current label? Yeah, thank you. So EPIDIOLEX now is the largest grossing epilepsy drug and has a very long exclusivity period into late 2030. So it makes us bullish on wanting to do more evidence generation and development there. The other characteristic that makes us pretty bullish is that it's very well tolerated and very combinable. And for many of the indications, patients are on multiple different drugs, and it's important to be able to combine drugs. We're also beginning to elucidate the non-seizure benefits as we've published on caregiver surveys showing perceived benefits on behavior, cognition, et cetera. We recently published an EpiCom study, which is one we did to look at behavior and cognition in TSC patients. So we think there are beyond seizure benefits. Now, the current indication for EPIDIOLEX is seizures associated with three different DEEs, Dravet, TSC, and LGS. While we do not promote on it, we certainly know that there is probably use beyond that because EPIDIOLEX certainly has activity across different types of seizure types. Our goal in the additional development programs that we recently announced is first to support the label indications with additional data. That includes the adult study in LGS. We are bringing forward a solid oral dose capsule, which may facilitate dosing in adults. Then to again, continue to generate data and get that message out that there are certain seizure types where EPIDIOLEX works particularly well. We are looking at a phase II in focal onset seizure. Then the next piece of this is actually expand the label into other orphan epilepsy, such as juvenile myoclonic epilepsy, where we are starting a phase II, phase III. Lastly, what seems to be happening in the field, you asked earlier about the pan-tumor trial and the tumor agnostic indication. Something similar is happening in epilepsy, where we know EPIDIOLEX is effective across a number of different seizure types, yet the indication is specific DEEs. We have approached the FDA to say, if we were to generate more data in DEEs outside those 3, could we have a broad label that just says any patient with epilepsy and DEE could get EPIDIOLEX? There was an openness to that in the same way that there was to a pan-tumor trial, provided that you show the evidence that it works broadly. We are initiating a trial that will enroll beyond those 3 DEEs that we already have an indication for, and hopefully that will help broaden our label there. Great. I know we are approaching time here. I will see if there are any questions from the audience. Otherwise, I can ask one to close us out. Over the next 5 years, sir, what do you think your mix is going to look like between oncology, epilepsy, and the rest? Yeah, great question. 2030 is right around the corner. I think about I started 8 years ago really coming to Jazz to help create a more innovative biopharma and build that pipeline. At that time, we had a real strength in narcolepsy and some rare oncology areas. It was hard to develop a strategy right then. It took us a little bit of time to figure out, "Well, where else can we go and be successful?" We are in a very different place now. For one thing, we have proven capabilities across an array of different rare diseases. I think that core capability underlies our strategy to say, "We have been a rare disease company, and we think we can continue to be successful in rare diseases," even if it means that we go out and branch into a different rare disease the way we did with epilepsy. In addition to that, we also have some real core strengths. Epilepsy, to me, and this underpins the deal we do with Actio, there is scientifically a renaissance happening in epilepsy. The way I experienced this in oncology was 30 years ago when the human genome was mapped. We then figured out all the oncogenic drivers in cancer, and we developed targeted therapies. This took a little longer in epilepsy, but now we know in many cases the genetic drivers for some of these rare epilepsies. The Actio deal in KCNT1 is a perfect example. It is a single gene that when it is mutated, causes epilepsy. We do that in mouse models. It is a gain of function, so it activates the potassium receptor, and so lends itself to a small molecule inhibitor, which Actio develops, a very targeted small molecule inhibitor with very little off-target activity. We also knew experimentally you could knock down that channel and have a benign phenotype, very little toxicity. You could take the gene out in mice entirely and see no problems. So we knew that the premise there was solid, and we were convinced that their molecule was effective based on pre-clinical data. By the time we finally did the deal, we saw clinical data that are not out there yet, but will be soon. For us, I think when you see it, you will agree that it represents a perfect example of the renaissance that is happening in epilepsy that we want to be part of. So building on EPIDIOLEX as a major platform, our existing pipeline, where we have absence epilepsy, and then we have another GGE play with the Kv7 molecule. Adding into that, Actio. To answer your question, I think we will continue to look for opportunities in epilepsy for sure. In sleep, there is less going on there, but still opportunities. Then, as I said before, I think we have an opportunity to have a best-in-class orexin. Then oncology. What a difference in the 8 years that I have been here. I think we showed we can do oncology well. We had a Lancet publication on the IMforte trial, which no one had really done before, gone into a maintenance setting in small cell lung cancer. There were a lot of people who said, "You're not going to be able to do it because patients don't want more chemotherapy after their induction." We did that well. We showed the benefit there, published in Lancet. We took an asset that I guess, frankly, others weren't seeing the value in, Ziihera. We executed on the plan that was in place, BTC, GEA, and we've expanded into other areas where I think there's a lot of potential. That now gives us a foothold in GI malignancy, sure. I think there's a lot of areas where we can then build on that and take lessons learned from that experience as well. That's a little bit of a framing around our rare disease strategy, building on the expertise and capabilities we have to really go into areas where Jazz, we're confident that we can compete. We think that will continue to transform and shape the pipeline through the 2030 period. Okay. Great. With that, we are at time. Rob and Jack, thanks so much for joining us. My pleasure. Thank you.