In in vivo CS-exposed mouse models, GPx4+/− mice showed remarkably higher levels of lipid peroxidation, non-apoptotic cell death, DAMPs release, and enhanced COPD phenotypes of airspace enlargement and small airway thickness relative to WT mice, all of which are attenuated in GPx4 TG mice. This evidence concerns the gene GPX4 and chronic obstructive pulmonary disease.