In the model of COPD established by exposure to CS, down-expression of GPX4 might ultimately induce iron accumulation and lipid peroxidation, which confirmed the key effect of ferroptosis on CS-induced COPD and further revealed the mechanism of iron accumulation inducing ferritinophagy mediated by NCOA4 in epithelial cells (81). This evidence concerns the gene GPX4 and chronic obstructive pulmonary disease.