The defect in STAT1 levels post-IFN-γ stimulation that we observed in our APECED patients is modest relative to the complete absence of STAT1 phosphorylation following IFN-γ stimulation in patients with IFN-γ receptor deficiency [(23); Figure 1A]. This evidence concerns the gene IFNG and hyperinsulinemic hypoglycemia, familial, 4.