While it is well established that impaired CFTR-mediated Cl− secretion and airway surface dehydration due to mutations in the CFTR gene cause cystic fibrosis (CF) with early onset and severe chronic obstructive airways disease [37]–[39], little is known about the relationship between endogenous variability of WT CFTR function and susceptibility for lung disease in humans. This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.