Several lines of evidence support the conclusion that CFTR is the major apical membrane Cl− pathway in secretory diarrheas caused by the bacterial enterotoxins in cholera and Traveler's diarrhea; (i) The small intestine and colon show robust cAMP-activated CFTR Cl− currents [30]; (ii) intestinal Cl− and fluid secretion are reduced in CFTR-deficient mice and humans [31]–[33]; and (iii) CFTR inhibitors are effective in various rodent models of cholera [18], [19]. This evidence concerns the gene CFTR and vibrio infectious disease.