TRAF3 and Autoimmunity: Specific deletion of the Traf3 gene from B lymphocytes in mice leads to prolonged B cell survival, constitutive NF-κB2 activation, augmented BCR signaling, elevated T-dependent and T-independent antibody responses, enhanced TLR responses, and increased IL-6-induced plasma cell differentiation, which culminate in autoimmunity and B lymphomagenesis (15–24).