The hallmark of the ABC subgroup of DLBCL is constitutive nuclear factor κB (NFкB) activation due to activation of the “CBM” signaling complex that consist of CARD11, BCL10 and MALT1, this complex may be constitutively stimulated by mutations of CARD11 and through chronic active B-cell receptor (BCR) signaling and downstream kinases including PI3K [18,19]. This evidence concerns the gene PIK3CB and aneurysmal bone cyst.