In our study, we found that antagonistic anti-CD154 blocked baseline phosphorylation of P65 and IκBα, as well as nuclear translocation of P65 and c-Rel in B cells from active lupus patients (Fig. 4), suggesting that, in active SLE patients, B cells express functionally activated CD154 and are involved in constitutive activation of NF-κB signaling pathway. This evidence concerns the gene NFKB1 and systemic lupus erythematosus.