Recent studies have reported that gain-of-function mutations in CLCN2 are linked to hyperaldosteronism (Fernandes-Rosa et al. 2018, Scholl et al. 2018), wherein enhanced ClC-2 channel function leads to cell depolarization and subsequent activation of voltage-gated calcium channels in the adrenal zona glomerulosa. Here, CLCN2 is linked to hyperaldosteronism.