Are there specific, um, things you can tell us about these, uh, targets, like, you know, uh, CALR versus the, you know, JAK2? Like, I mean, is, is there any- anything unique about them from a target perspective, the way they work, the way they lead to disease proliferation, or it just happens to be something that we see in one disease versus another?

No, there are actually some important differences and differences that impact drug development, to your point.

So, for example, CALR, uh, granted it only accounts for a quarter to maybe thirty percent of ET and, and PMF, but CALR, uh, is actually expressed on the cell surface because of the mutation.

So it is a, it's an intracellular protein.

It's actually an endoplasmic reticulum chaperone.

Uh, but because of the mutation, it comes outside the cell, and that allows all these immunotherapy approaches.

So, you know, there are, um, you know, there's an antibody that's, that we already have results on.

And I wanna talk a bit about endpoints later on because it matters for a phase three trial, the endpoints for-