In these models of gliadin sensitivity, pretreatment with the CFTR potentiator Ivacaftor, a drug approved for the treatment of CF patients bearing particular CFTR mutations [5, 43], prevents the gliadin-induced suppression of the CFTR-mediated chloride current (as observable in the small intestine mounted in Ussing chambers responding to the CFTR stimulator forskolin) and controls the gliadin-induced intestinal inflammation. The gene discussed is CFTR; the disease is cystic fibrosis.