They showed that in vitro CTLA-4 down-modulation increases the proliferation rate of leukemic cells and upregulates surface expression of CD38, a well-known marker of high-risk CLL, together with the expression of STAT1, NFATC2 and c-Myc, which represent downstream molecules of the B-cell proliferation/survival signaling pathway [50]. The gene discussed is CTLA4; the disease is B-cell chronic lymphocytic leukemia.