It has been well recognized that IL‐36γ agonizes and IL‐36Ra antagonizes IL‐36R‐mediated activation of NF‐κB and induction of proinflammatory cytokines and chemokines in cells in vitro.[23, 42] However, the levels of total and phosphorylated (p) p65 were comparable between the control and the IL‐36γ KO or the IL‐36Ra KO tumors (data not shown), indicating that knockout of IL‐36γ or IL‐36Ra had minimal effect on the activation or expression of NF‐κB in the tumor tissues. The gene discussed is IL1RL2; the disease is neoplasm.