The ablation of ClC-2 in a different Clcn2−/− mouse model led to an increase in cAMP-dependent Cl− secretion, and double mutants lacking ClC-2 and expressing the CF mutant CFTR-ΔF08 had a markedly decreased early lethality [14], presumably due to an alleviation of the intestinal obstruction that normally takes place in CF animals owing to decreased fluid secretion. The gene discussed is CFTR; the disease is cystic fibrosis.