Aberrant activation of nuclear factor-kappaB (NF-κB), either through the “canonical” pathway activating p50/p65 and p50/c-Rel dimers, or through the “non-canonical” pathway activating p52/RelB dimers, has been associated with tumor proliferation and survival in DLBCL, especially in the ABC subtype [1, 2]. The gene discussed is CD40; the disease is neoplasm.