 I guess I only left a couple of minutes here, but I'm certainly happy to take any questions. And I'm gonna open up the Q&A and see if anything's here. All right, so our first question, is it possible we use diagnostic pheochromosatoma with F-18, eftopa, and go on therapy with MIBG, both tracers on the same mechanism of uptake and kind of cold mean metabolism? I think that's a really interesting idea. And I don't disagree that you can potentially confirm a target expression with something that may be different than the actual agent that you're treating with. And I think we maybe even see that with say the PSMA agents. Chemically, something like F-18, DCFP, YL is distinctly different than something like lutecium dotitate, although they have one sort of moiety in common and that moiety drives the binding of both. So yeah, I don't think we necessarily have to feel kind of chemically constrained to have the exact same molecule. My concern would be more what our source of I131 MIBG is going to be going forward. So that may be kind of more of the problem than what we select with. And then a second question, in your experience, the best time for an F-18 PSMA scan, 90 or 120 minutes, we have issues of bladder and ureter uptake. Yeah, so a couple of things I'm packed there. So there is some data that as you go to later and later time points post injection, you can potentially find subtle things that may have missed at earlier time points. I will say the label in the US is, I think anywhere from 45 up to 90 minutes, I may not have those numbers exactly right. We do tend to scan at one hour at my institution, only because it fits in very neatly with the F-18 FDG workflow that sort of dominates our oncology practice. So I think there are sort of practical advantages to one hour. I do think you may find some subtle things as you go out to those later time points. And I wish I had the flexibility of my pet center to potentially go to those later time points. And in terms of bladder and ureter, yeah, absolutely, it can be tough to read around those. So there are places that give Lasix. We don't, and that's partly because, particularly our patients who are post-prostatectomy, they're already having trouble holding their urine. You hit them, wallop them with a dose of Lasix and you're gonna wind up with a lot of radioactive urine on your pet scanner, all likelihood. So we don't do that, although people do and I don't think it's unreasonable. There have been cities then where patients are catheterized. I can tell you if you take most minimal prostate cancer, they're not gonna want you to put a catheter in them. So we kind of just do our best. We have the patient void right before they get on the table and then we started our acquisition from the bed thighs. So hopefully we're only a couple of minutes, a couple of minutes post their last urination by the time we hit the pelvis. And hopefully that minimizes the amount of, at least urine in the bladder that you have to contend with. With the ureters, it can be challenging. I think it's very incumbent upon us in terms of anatomy to make sure we've got the anatomy right. And then you can potentially, if you're really stuck on ureter versus a lymph node, if you have the flexibility, you could also go and reacquire the pelvis to kind of make sure that if it moves, it must have been ureter. And if it's still there, it's probably a lymph node. Couple more questions and I'll try to get through these fairly quickly. So is it might be G more sensitive than gallium dodetate and neuroblastoma? I don't believe so. I think gallium dodetate is what we're eventually, eventually going to all be doing, although that is not the guidelines recommendation in the U.S. right now. I think in Europe, a lot of those patients are now in an issue with dodetate. And then one last question. Any thoughts on FAPI agents and their promise? Yes, I think FAPI as a diagnostic tool is definitely on the horizon and I hope we have widespread access to it in the very near future. I remain unsure what its ultimate therapeutic applications might be. I fear that when we go and we basically wipe out the cancer associated fibroblasts, that at least some of those cancer associated fibroblasts may be kind of holding the tumor at bay and we don't necessarily understand enough about the biology to know if that's a good thing or a bad thing. So those all remains to be seen, but I agree the fibroblast activating protein, both inhibitors and other things that bind to that, I think are super promising. I do apologize. I think we're a minute or two over time. So I think I'll probably have to kind of stop answering questions, but I really appreciate everyone logging in and it was really a pleasure to speak with you all today and hope to see you back here in the not too distant future. So thank you all again. Hope everyone has a great day.