Previous studies reported elevated mitochondrial accumulation of PINK1 and reduction of Parkin expression in COPD lungs, but not in non-COPD smokers, suggesting that an increase in PINK1/Parkin ratio is not only dependent on smoking status but correlates with COPD pathogenesis (Figure 3) [41, 60, 62]. This evidence concerns the gene PRKN and chronic obstructive pulmonary disease.