In our study, we found that the local decline of IL-38, and the concomitant induction of IL-36γ and IL-36Ra in psoriatic epidermis, are common to other inflammatory skin diseases characterized by a prominent neutrophilic infiltrate, including not only HS, but also Sweet’s syndrome and PG, where an altered epidermal architecture has been reported38,39. The gene discussed is IL36G; the disease is sweet syndrome.