Additionally, we found that hypermethylated mitochondrial inner membrane protein like (MPV17L; +194 CpG site) gene was associated with rapid lung function decline in all the COPD patients, while in vitro demethylation agent, 5-aza-2′-deoxycytidine, treatment in THP-1 cells reversed CSE and OVA co-exposure-induced promoter hypermethylation-mediated MPV17L under-expression, as well as ameliorated cell apoptosis and oxidative stress. This evidence concerns the gene MPV17L and chronic obstructive pulmonary disease.