One recurrent mechanism to activate NF-κB in ABC DLBCL is chronic active B cell receptor (BCR) signaling [4], which is initiated by self-antigen reactivity of the BCR and is augmented by gain-of-function mutations in the BCR subunits CD79A and CD79B in ∼21% of cases [4, 7]. The gene discussed is CD79A; the disease is aneurysmal bone cyst.