In airway and alveolar epithelium, METTL3 targets SOCS3/STAT3, ACSL4, KCNH6, PTEN and others to promote epithelial–mesenchymal transition, ferroptosis and barrier disruption, thereby tightly coupling inflammatory signaling to structural remodeling in COPD, pulmonary fibrosis and ALI/ARDS. This evidence concerns the gene STAT3 and chronic obstructive pulmonary disease.