CACNA1H and adrenal cortex adenoma: In vitro studies have demonstrated that gain-of-function variants of CACNA1H, when stimulated by potassium, lead to over-expression of CYP11B2. The prevalence of somatic CACNA1H mutations in aldosterone-producing adrenocortical adenomas is 4%, and it is unclear whether these mutations play a role in cell proliferation in aldosterone-producing adrenocortical adenomas besides determining the hormonal hypersecretion [58, 95, 96].