Examples include Liddle’s syndrome, with an activating mutation of epithelial Na channel (ENaC); two types of Gordon’s syndrome, with mutations in two regulatory kinases [with no lysine (K) serine/threonine protein kinases (WNK)1 or WNK4]; and apparent mineralocorticoid excess (AME), with an inactivating mutation in the glucocorticoid-metabolizing 11β-hydroxysteroid dehydrogenase type 2 enzyme (11HD2). This evidence concerns the gene WNK4 and Increased circulating aldosterone concentration.