Auto-Abs against IL-17A and IL-17F (and IL-22) have been reported to underlie chronic mucocutaneous candidiasis (CMC) in patients with autoimmune polyendocrine syndrome type 1 (APS-1), paving the way for the identification of inborn errors of IL-17 immunity in patients with isolated or syndromic CMC (e.g., AD IL-17F, AR IL-17RA, AR IL-17RC, AR ACT1, AD MAPK8, AR IL-23R, AR c-Rel, and AR ZNF341 deficiencies, or AD STAT1 gain-of-function [GOF]) [13–15]. The gene discussed is TRAF3IP2; the disease is autoimmune polyendocrine syndrome type 1.