 This disease that my mom had, cesare syndrome, it's a cancer that arises from your cutaneous T cells. The cancer that we were analyzing here is a lymphoma. Lymphoma is a cancer of T lymphocytes. T lymphocytes normally are regulated very closely within the immune system in terms of what allows them to grow, to proliferate, and what controls them and prevents that growth and keeps it in check. The issue I faced was my mother had wonderful doctors there in Kentucky. I had a wonderful technical team who was going to generate the raw data for us to see what was in her genome, but I didn't have anybody on my team that could connect those two things. The TGEN group, working with Dr. Sekulik, found every single finding that mattered in my mom's clinical case. My role focused on taking all the raw data, which consists of millions and millions, and I guess somewhere around a billion or so small reads that are 100 letters a piece and mapping them back to genome to identify those differences unique to the tumor that was taking over her. I was the informatics aspect. The biology aspects, interpreting what it means to have an amplification or a tendon duplication of CTLA4, CD28, the biology of that. For that, I had my partners, John Carpenter and Alex Sekulik, Tim McDaniel. We got the data, we performed our analysis, and something floated up to the top. There is a gene on chromosome 2 that controls the growth of T cells, and that gene was altered in the tumor, what we call a fusion, where two aberrant genes fuse together to form a protein that should not be expressed in the cell. And that protein makes a T cell want to grow and continue to grow and never stop growing, which is essentially the foundation of a lymphoma. What the tumor did is it actually put the extracellular component of CTLA4, the inhibitor, fused it to the intracellular portion of CD28, which is the activator. So every time you try to stop that cell, you basically just accelerate more. The FDA had just approved a drug called ipilumamab to target one of the partners of this fusion. That blocker now would block, we reasoned, not a true CTLA4, but it's not blocking a break, it's blocking a new driver. And as my mother stepped into Dr. Goman's office one week after her first infusion, he took one look at her and he could immediately see that something had changed. Instead of being red, her skin was now a much more healthy pink color. Just in that short time, all the tumors in her body started closing, shrinking in size and getting better. It was immediately apparent that something was going on following the treatment with this drug that the genome had identified. We don't know how common the CTLA4-CD28 fusion is, how important it is in driving other cancers, but this way we can basically put out there and say, we saw this event, we identified a therapy, the patient went on the therapy, the patient had a response. Those are all important things. The question is, is that seen elsewhere? Within about two months of that first infusion, the disease started coming back and when it came back, it was fairly rapid. And by the end of November of that year, my mother succumbed to the disease. You look back on it and you think, if only we had had that drug and if only we had had the sequencing, when my mother was first diagnosed, on the other hand, you can think how lucky we were that she happened to be there right at that moment in time when all of this was first possible. And you can also look at her case and see it just as a little glimpse of what's going to be possible for patients to come.