Furthermore, our attempt to understand the biology of CD5+ DLBCL suggested that molecular pathways downstream BCR signaling which promote cell proliferation and survival (such as Bcl-2 [but not Myc] overexpression, and activation of c-Rel, p65, and STAT3) were likely relevant for the pathogenesis of CD5+ DLBCL; however, the adverse impact of CD5 expression did not depend on any of these factors alone. The gene discussed is STAT3; the disease is diffuse large B-cell lymphoma.