These findings raise numerous questions about this anti-IFN response in APS1 patients that we now address; they concern its kinetics, its specificity for different IFN-α subtypes, other IFNs, and other cytokines, its specificity for APS1 versus its component diseases, its correlation with the various AIRE genotypes, and the mechanisms of autoimmunisation. This evidence concerns the gene IFNA2 and autoimmune polyendocrine syndrome type 1.