Following the equilibration in the presence of amiloride and indomethacin, CF tissues were stimulated with IBMX and forskolin to achieve maximal activation of luminal CFTR Cl− channels and basolateral KCNQ1/KCNE3 K+ channels, and co-stimulated with CCH to activate Ca2+-regulated KCNN4 K+ channels, thus maximizing the driving force for CFTR-mediated Cl- secretion [8], [19]. The gene discussed is KCNQ1; the disease is cystic fibrosis.