One of the consequences of TRAF3 deficiency (presumably attributed to the NF-kB2 over-activation) is the expansion of marginal zone (MZ) B cells (13, 17), which might explain the hyperreactivity to TLR ligands (18) and the systemic lupus erythematosus (SLE)-like autoimmunity observed in these mice (13). Here, NFKB2 is linked to systemic lupus erythematosus.