The central role of IL-17 cytokines in mucocutaneous immunity to Candida has been supported by descriptions of the autosomal dominant hyper IgE syndrome [69], CARD9 deficiency [70] and dectin-1 deficiency [71], all of which are associated with impaired Th17 cell development and susceptibility to mucocutaneous candidiasis, as well as mutations in the genes encoding IL-17 receptor A (IL-17RA) and IL-17F in patients with CMC [72]. This evidence concerns the gene IL17RA and hyperinsulinemic hypoglycemia, familial, 4.