Since IL-17 stimulates the production of keratinocyte-produced antimicrobial peptides such as human beta-defensin-2 and catelicidin (LL-37), and also promotes neutrophil recruitment, the inhibition of IL-17A, IL-17 and the heterodimer IL-17A/F may reduce mucocutaneous innate immunity and, thus, predispose to superficial dermatophytosis. The gene discussed is CAMP; the disease is dermatophytosis.