The abnormal activation of the type I interferon (IFN) pathway has received particular attention for its role in the pathogenic mechanisms underlying SLE; the role of this pathway was initially demonstrated by the induction of a signature of IFN inducible genes in human monocytes exposed to SLE sera [6] and then further corroborated by gene expression microarray studies of peripheral blood cells in SLE [7–10]. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.