Individuals with primary immunodeficiencies resulting in defective Th17 immunity, such as STAT3 loss-of-function (LOF) mutations in autosomal-dominant hyper-IgE syndrome, STAT1 gain-of-function mutations, RORC LOF mutations, or CARD9 LOF mutations show a strongly increased risk of developing chronic mucocutaneous candidiasis (CMC).22–30 Genetic defects in the IL-17 pathway itself, such as mutations in the IL-17 receptor A (IL-17RA) or IL-17RC subunits, in the signaling component Act1 or in the cytokine IL-17F were also found to underlie CMC.31–33. This evidence concerns the gene STAT3 and Chronic mucocutaneous candidosis.