Since ENaC activity is regulated by mediators present in the ASL (e.g., nucleotides and proteases [27],[28]), and Ussing chamber (“thick-film”) studies result in washing away of these critical ENaC regulatory factors, we determined how CFTR delivery to CF ciliated cells affected the regulated activity of ENaC under thin-film conditions using microelectrodes. The gene discussed is CFTR; the disease is cystic fibrosis.