These studies have suggested IL-17–centric pathogenesis, supported by the role of IL-17A in psoriasis as one of the most highly enriched biological processes in HS skin, followed by interferon signaling (11), and are consistent with findings from our own group that showed increased protein levels of IL-17A and to a lesser extent IFN-γ in lesional HS skin (12). This evidence concerns the gene IL17A and psoriasis.