These advances included the characterization of mutant BCL10 and MALT1 proteins caused by chromosomal translocations leading to constitutive/aberrant NF-κB signaling in lymphoma (7), the discovery of CARD11 and its ability to interact with and regulate BCL10 (8), and the identification of mutant CARD11 isoforms affecting the coiled-coil domain that activate NF-κB, constituting ~10% of activated B cell-like diffuse large B cell lymphomas (9, 10). This evidence concerns the gene NFKB1 and lymphoma.