These findings indicate that uncontrolled NF-κB signaling caused by the loss of A20 function is involved in the pathogenesis of B cell lymphoma subsets, and they strongly suggest a tumor suppressor role for A20, the loss of which may contribute to B cell lymphoma pathogenesis by causing supra-physiological NF-κB activation, which, in turn, has oncogenic properties including inhibiting apoptosis and promoting cell proliferation[28,33]. Here, TNFAIP3 is linked to neoplasm.