This may also have potential for impact beyond the world of CF, given that it is now well established that acquired CFTR dysfunction is an important feature of smoking-related lung diseases, with evidence that cigarette smoke can impair bacterial phagocytosis in a CFTR-dependent manner in RAW264.7 cells, while CFTR modulators can improve the “CF-like” clinical feature (mucus thickness/stasis and bronchiectasis) of animal models of Chronic Obstructive Pulmonary Disease (COPD) (72–75). This evidence concerns the gene CFTR and bronchiectasis.