While some scattered evidence indicated the potential role of type I interferon in lupus, several observations did not support the hypothesis: first, not every SLE patient has detectable serum type I IFN levels [27]; second, dysregulation of type-I IFN production is not found in most murine SLE-models [28]; and third, genetic linkage and association studies had not identified candidate lupus susceptibility genes within the IFN pathway [29]. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.