There are other monogenic forms of hyperaldosteronism due to excess adrenal production of mineralocorticoid related to variation in CYP11B1 (glucocorticoid-remediable aldosteronism), CLCN2, KCNJ5 and CACNA1H that phenocopy these intra-kidney forms of apparent mineralocorticoid excess, though manifest with extra-kidney features of hyperaldosteronism [36–39]. This evidence concerns the gene CLCN2 and hyperaldosteronism.