Known forms are inherited in an autosomal−dominant fashion and include familial hyperaldosteronism type I (FH-I) with mutations in CYP11B2 (aldosterone synthase)17,18, FH-III due to mutations in the potassium channel KCNJ59,19 and FH-IV caused by mutations in the T-type voltage-gated calcium channel CACNA1H20,21. This evidence concerns the gene KCNA3 and glucocorticoid-remediable aldosteronism.