These constitutive activations, characterizing ABC DLBCLs, are related to somatic gain of function mutations and/or duplications affecting positive regulators of this pathway such as CD79a and CD79b [12], MYD88 [13], CARD11 [14], TRAF2, TRAF5, MAP3K7/TAK1 and TNFRSF11A/RANK [15] or somatic inactivating mutations and/or deletions of negative regulators such as TNFAIP3/A20 [15,16]. This evidence concerns the gene MAP3K7 and aneurysmal bone cyst.