However, our results in neonatal and adult βENaC-overexpressing mice on different genetic backgrounds (C57BL/6, BALB/c and CFTR−/−) (Fig. 4,5 and Fig. S3) also indicate that pharmacological augmentation of CFTR function may be more effective in the early pathogenesis, and that late treatment may not be able to correct or revert established COPD with chronic mucus hypersecretion, airways inflammation and emphysema. This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.