Constitutive MALT1 protease activity and the capacity of cIAP2-MALT1 to potently activate both the canonical NF-κB1 (via the MALT1-dependent recruitment of TRAF6 and proteolytic inactivation of A20) and non-canonical NF-κB2 pathways (discussed in Section 5) drive the growth of these MALT lymphomas [24,107,121,148,149]. This evidence concerns the gene BIRC3 and MALT lymphoma.