It has been reported that Il1rl2−/− mice exhibit reduced disease severity in an acute DSS‐induced model of colitis,[52] whereas the same mice are sensitive to DSS‐induced colitis and exhibit impaired IL‐22 production and mucosal healing in the colon.[29, 30] Considering that IL‐36R is widely expressed in various types of cells including epithelial cells, fibroblasts, T cells, and neutrophils,[33] the discrepancies among these studies might be due to different functions of IL‐36R in distinct types of cells. The gene discussed is IL22; the disease is colitis.