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]. This evidence concerns the gene BCR and aneurysmal bone cyst.