 Five years ago, we started doing genomic sequencing to understand what mutations are driving the cancer. Foundation 1 was the first that, but that required a biopsy. Just over the last two or three years, we've got more and more liquid biopsies, so you don't have to have an invasive surgery to pull part of the cancer out of your lung. You can just do a blood draw. And based on that, you can understand, okay, this is the mutation likely driving my cancer, and this is the treatment. What I think is the next step is realizing it doesn't necessarily have to be lung cancer versus colon cancer versus prostate. It's all based on the mutation. So, if you have a RAP mutation, yes, RAP inhibitors are proved in colon cancer, but if you only have a RAP mutation in its lung cancer or prostate, that's probably the right drug for you. Because cancer really doesn't care where it originates, it only cares what the mutation that drives it is. If you can block that mutation, you can pull a cancer out by its roots, and you can have just marvelous clinical outcomes. For sure. And I think that applies definitely to a lot of cases. I wish it was everyone, so that's yet to be determined. But you touched on two very big points, and that is, when we're going to precision therapy, we're talking about what is the driver? What is the person that revs that engine up to six or seventh gear and makes that thing propagate in an unregulated way? And what we're learning is there are mutations, that driver mutation, that basically if we can neutralize it, then that propagation cannot happen. And that is precision and targeted therapy. And it's used as a term that I'm very excited about that I don't think is the mainstay yet, but the term is tissue agnostic. What does tissue agnostic mutation or driver mean? That means that it does not matter. The way we always look at cancers and still do all the time is histopathology. What that means is you take a piece of the tissue, you throw it on the slide, you stain it, and you say, it looks like adenote, it looks like squamous. And that was important because for whatever reason, like an adenocarcinoma and the colon may not behave the same way as an adenocarcinoma alone. So it was very important for the tools we had, which was cytotoxic chemos, the poison-ish chemos that people think about. Now we're realizing, yo, it doesn't really matter what's on this slide, as far as the histopathology goes. It's more because now we're at a molecular level, we're not looking at the conglomerate cells, but inside to actually look at the pieces and all the switches, we're like, whoa, it gives me goosebumps still thinking about it. We can actually stay with the target. It doesn't matter what it is, it can respond. That's right. And that's amazing. Yeah, that's correct. And the really nice thing is I feel like we're getting into an area where you'll get a bifurcation. If you present with cancer, you do NGS, you do genomic sequencing, I should say. If you have one or two mutations, then hopefully we will have developed a precision man that can go after the thing that's causing the cancer, block it, get a great outcome for the patient. If you have a lot of mutations, hey, immuno-oncology works well for you then, because if you have a lot of mutations, the cancer doesn't look like self and your immune system will react to it.