Familial hyperaldosteronism type I (FH-I) occurs by an unequal crossing-over of the genes encoding steroid 11β-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2), resulting in a chimeric CYP11B1/B2 gene that produces an enzyme with aldosterone synthase activity with ectopic expression in the zona fasciculata, which is regulated by plasma adrenocorticotrophic hormone (ACTH) levels instead of by angiotensin II [6-8]. The gene discussed is AGT; the disease is glucocorticoid-remediable aldosteronism.