IL-36 combined with IL-1 to recruit neutrophils in the dermis and epidermis and, then, promoted the inflammatory keratinocyte response via inducing the expression of inflammatory chemokines, such as IL-8 (45), suggesting that the IL-36/IL-1–chemokine–neutrophil axis may have a role in the pathogenesis of psoriasis. The gene discussed is IL1B; the disease is psoriasis.