These results, together with the observation that expression of the pro-inflammatory cytokines KC and TNF-α were elevated to similar levels in βENaC-Tg mice on both genetic backgrounds as early as 3 days of age (Fig. S2), suggests that the endogenous difference in CFTR activity (∼2-fold) between airway tissues from C57BL/6 and BALB/c mice was not sufficient to prevent long-term consequences and secondary pathologies, including airway inflammation, mucus hypersecretion, goblet cell metaplasia and emphysema triggered by airway surface dehydration in βENaC-Tg mice in vivo[4], [13]. This evidence concerns the gene TNF and pulmonary emphysema.