Currently, it is generally believed that the immune‐inflammatory cascade mediated by the immune cell function and the release of inflammatory factors (e.g., tumor necrosis factor‐alpha [TNF‐α], interleukin‐1beta [IL‐1β], IL‐23, and IL‐12) are closely implicated in the onset and progression of psoriasis despite its inexact pathogenesis.4, 5. Here, IL1B is linked to psoriasis.