In line with the experimental data observed in the M. canis mouse model, patients with mutations that lead to the gain of function in the transcription factor STAT1 (STAT1 GOF), that promote type I and type II IFN genes transcription, have reduced type 17 immunity and are susceptible to chronic mucocutaneous candidiasis (CMC) and dermatophytosis (96, 97, 114–117). This evidence concerns the gene STAT1 and chronic mucocutaneous candidiasis.