However, in contrast with the findings in βENaC-Tg/NE−/− mice, neither genetic deletion nor pharmacological inhibition of MMP12 reduced airway inflammation or goblet cell metaplasia in βENaC-Tg mice indicating that MMP12 is not essential in the in vivo pathogenesis of CF-like airway diseases [52]. This evidence concerns the gene MMP12 and cystic fibrosis.