Araya et al. discovered that, compared with wild-type COPD mice, parkin RBR E3 ubiquitin protein ligase (PRKN) gene-knockout mice exhibited a more substantial accumulation of damaged mitochondria, cellular senescence, airway wall thickening, emphysema lesions, and inflammatory response after exposure to CS for 6 months (Araya et al., 2019). This evidence concerns the gene PRKN and chronic obstructive pulmonary disease.