In summary, we demonstrated that CD40-induced NF-κB signaling was constitutively activated in B cells from active lupus patients, including increased phosphorylation and degradation of IκBα, phosphorylation of P65, as well as increased nuclear translocation of P65, P50, c-Rel, which could be blocked by antagonistic anti-CD154. The gene discussed is NFKB1; the disease is systemic lupus erythematosus.