The acquired loss of the cystic fibrosis transmembrane conductance regulator (CFTR) function, a chloride and bicarbonate-selective, 3′,5′-cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) regulated anion channel4, is invoked in the pathogenesis of COPD partly as a consequence of CS exposure5,6. Here, CFTR is linked to chronic obstructive pulmonary disease.