Consistent with these findings, a subsequent independent study demonstrated that an upstream CD31-CD38 signaling axis in trans between stromal and leukemic cells of CLL patients actually led to SEMA4D/CD100 up-regulation, promoting leukemia cell viability through Plexin-B1 found in stromal cells, as well as a concomitant decrease in the expression of CD72 negative regulator of immunity (10). The gene discussed is PLXNB1; the disease is B-cell chronic lymphocytic leukemia.