A recent study on the effects and mechanism of GSNO augmentation in regulating inflammatory oxidative stress and COPD emphysema pathogenesis demonstrated that CFTR-colocalized aggresome bodies were correlated with an increasing emphysema severity in the lung of COPD subjects, and the treatment of GSNO or GSNOR inhibitor (N6022) could significantly inhibit cigarette smoke extract (CSE)-induced decrease of membrane CFTR, through a mechanism that involves rescuing CFTR from ubiquitin (Ub)-positive aggresome bodies and inhibiting CFTR protein misfolding. This evidence concerns the gene ADH5 and chronic obstructive pulmonary disease.