The most striking finding of the current studies was that PBMC from inactive SLE patients with normal serum IFNαα levels, have constitutive phosphorylation of IFNAR signaling molecules, which is not explained by intrinsic hypersensitivity to ligand binding as an exogenous IFNβ induced similar phosphorylation of Jak1 and STAT2 in SLE and control PBMC. This evidence concerns the gene IFNAR1 and systemic lupus erythematosus.