Early studies (Kunzelmann et al., 1995; Stutts et al., 1995; Ismailov et al., 1996; Matsui et al., 1998; Tarran et al., 2005) proposed a popular mechanism by which the loss of CFTR function in CF epithelia might enhance ENaC activity, resulting in excess NaCl and water absorption, followed by reduced ASL height that impairs both the mucociliary clearance mechanism and bacterial eradication from the airway surface. Here, CFTR is linked to cystic fibrosis.