Furthermore, using a preclinical COPD-emphysema murine model, we demonstrated that chronic CS (Ch-CS) induced an increase in inflammatory cytokines in BALF, aggresome formation, CFTR-aggresome localization, oxidative/nitrosative stress, and apoptosis, and the emphysematous changes (alveolar airspace enlargement) were significantly improved by augmenting the airway GSNO levels [62]. This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.