These temporal and spatial differences are expected to result in a faster and more widespread deletion of Nedd4-2 in the neonatal vs. adult lung that may aggravate increased ENaC activity and mucociliary dysfunction, increased pro-fibrotic TGFβ signaling and potentially other pathogenic processes induced by Nedd4-2 deficiency [1,2,3,8,9,10,11,44,45,46,47,48,49]; therefore, they might also contribute to the more rapid onset and progression of ILD in congenital vs. conditional Nedd4-2−/− mice. Here, NEDD4L is linked to interstitial lung disease.