Excessive ROS induces oxidative stress that leads to aberrant oxidation of lipids, proteins, and nucleic acids and promotes cell death.[17] Consistently with the notion that IL‐36γ upregulated GSH levels to neutralize ROS which was antagonized by IL‐36Ra, the lung tumor cells from IL‐36γ‐ or IL‐36Ra‐deficient NSCLC mouse models were more or less prone to death than the controls, respectively. The gene discussed is IL36G; the disease is non-small cell lung carcinoma.