Scholl et al. compared CACNA1H missense mutations observed in primary aldosteronism to wild-type CACNA1H in a patch clamp experiment and observed that the mutated cells left-shifted, thus obtaining a lower threshold for activation and an almost ten-fold slower inactivation than wild-type channels, thereby increasing the secretion of aldosterone (Scholl et al. 2015). Here, CACNA1H is linked to primary aldosteronism.