In most of these cancers, NF-κB is frequently activated by recurrent genetic mutations targeting core components of the B Cell Receptor (BCR) complex, such as CD79A and CD79B, or upstream regulators of the canonical NF-κB pathway, such as MYD88, CARD11, and TNFAIP3/A20 [89,90]. This evidence concerns the gene NFKB1 and cancer.