First, the high IFNα levels usually present in SLE patients could be responsible for widespread leukocyte activation and induction of BLyS, as was suggested by the coordinated overexpression of IFNAR1 and BLyS on the membrane of B cells, monocytes, mDCs and neutrophils, and by the positive correlation detected between serum levels of both cytokines. This evidence concerns the gene TNFSF13B and systemic lupus erythematosus.