Increased activity of the epithelial sodium channel (ENaC) is the final common abnormality in several forms of hypertension: primary aldosteronism, glucocorticoid remediable aldosteronism, Liddle’s syndrome and 11-β-hydroxysteroid dehydrogenase-2 deficiency.1 Activating mutations of either the β- or γ-ENaC subunits can result in Liddle’s syndrome,2,3 in which constitutive reabsorption of sodium leads to hypertension and hypokalaemia in the presence of low plasma levels of renin and aldosterone. This evidence concerns the gene REN and Liddle syndrome.