Molecular studies have shownthat CD5 is a negative regulator of B-cell receptor signaling,8 modifies intracellular calcium, and modulates B-cell physiology by activatingvarious signaling pathways, including ERK1/2, PI3K, and calcineurin.9 CD5 also adds to B-cells survival advantage through stimulation of autocrineinterluekin-10 production.10 The mechanism leading to overexpression of CD5 in DLBCL remains unclear. The gene discussed is MAPK3; the disease is diffuse large B-cell lymphoma.