In CS-exposed GPx4+/− mice, remarkably high levels of lipid peroxidation, non-apoptotic cell death, DAMP release, and enhanced COPD phenotypes of airspace enlargement and small airway thickness were observed (relative to wild type mice), all of which are attenuated in GPx4 overexpressing mice [55]. Here, GPX4 is linked to chronic obstructive pulmonary disease.