In the light of the genetic defects of the K+ channel KCNJ5, Ca2+ channels, and ion-transporting ATPases that are causative factors for the formation of aldosterone-producing adenomas [42], it is surprising that the depolarized adrenal cortex of Task1 and Task3 knockout animals doesn’t show adenomas or overt adrenal hyperplasia. Here, KCNK3 is linked to congenital adrenal hyperplasia.