In addition, increased aggresome bodies were also found in the lungs of smokers and COPD patients, which were correlated with the severity of emphysema and alveolar senescence, suggesting that cysteamine was capable of modulating the cigarette-induced pathogenesis of the emphysema phenotype of COPD by restoring impaired autophagy and CFTR function [17, 69, 70]. The gene discussed is CFTR; the disease is pulmonary emphysema.