The hyperaldosteronism results in a massive colonic upregulation of the absorptive sodium transporter NHE3 (SLC9A3) and the epithelial sodium channel ENaC (6) However, whereas slc9a3−/− mice maintain a pelleted stool despite hyperaldosteronism accompanied by colonic upregulation of ENaC, slc26a3−/− mice and CLD patients have persistent, watery, chloride-rich stool leading (in mice) to premature death. The gene discussed is SLC26A3; the disease is hyperaldosteronism.