One hallmark of ABC-DLBCL is a constitutive activation of the NF-κB pathway (99) due to (i) mutations in NF-κB components CARD11 (100), A20 (101) or Myd88 (102) and/or (ii) chronic activation of the B-Cell Receptor (BCR) (as a result of mutations of in the BCR subunits CD79A/B) and downstream kinases (103, 104). This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.