SLC26A4 and Hypokalemia: As the Cl﻿−/HCO3− exchanger pendrin (Slc26a4) represents the exclusive apical route for renal HCO3− secretion and Cl﻿− retention, we questioned whether a loss of pendrin activation represents the cellular mechanism leading to the life-threatening condition with hypochloremic alkalosis, massive hypokalemia, and volume loss in alkali-loaded and salt-depleted Ae4−/− mice.