Glucocorticoid-Remediable Aldosteronism (GRA), or familial hyperaldosteronism type 1 (FH-1) results from an unequal crossing over between CYP11B1 (encoding for 11 β-hydroxylase) and CYP11B2 (encoding for aldosterone synthase), leading to ACTH-dependent aldosterone secretion, HTN, hypokalemia, low renin and high aldosterone levels. The gene discussed is POMC; the disease is glucocorticoid-remediable aldosteronism.