Because lung disease in βENaC-Tg mice is caused by a dysbalance between absorption and secretion of NaCl and fluid across airway surfaces, a focus of our studies was on the impact of the genetic background on ENaC-mediated Na+ transport and Cl− secretion mediated by CFTR and Ca2+−activated Cl− channels (CaCC) in freshly excised airway tissues. This evidence concerns the gene CFTR and lung disorder.