However, aldosterone and Sgk1 can stimulate ENaC independently of Nedd4-2 and their role in Liddle syndrome is controversial: aldosterone and Sgk1 were found to increase cell surface abundance of ENaC channels bearing Liddle syndrome deletions/mutations (which cannot bind Nedd4-2) [65-68] and, importantly, CCTs harvested from mutant mice bearing a Liddle syndrome deletion [52] revealed a normal response to aldosterone [69]. Here, NEDD4L is linked to Liddle syndrome.