Gao et al. [167] demonstrated that disulfiram (DSF) directly targets GSDMD and, through covalent binding, prohibits the pore-forming activity of its N-terminal fragment (GSDMD-NT), thus preserving airway epithelial barrier integrity and attenuating ozone-induced COPD pathology and lung function impairment. The gene discussed is GSDMD; the disease is chronic obstructive pulmonary disease.