To establish that exposure to cigarette smoke inhibits CFTR-dependent ion transport in our model, we exposed the apical surfaces of fully differentiated primary airway epithelial cells (HBE) derived from non-CF (wild-type) donors to increasing concentrations of organically soluble CSE, mimicking exposure levels in cigarette smokers [30], [31], [32]. The gene discussed is CFTR; the disease is cystic fibrosis.