CYP11B2 encodes aldosterone synthase, a mitochondrial cytochrome P450 monooxygenase that catalyzes the final three oxidative steps of aldosterone biosynthesis from 11-deoxycorticosterone, converting it sequentially through 11-beta-hydroxylation and two C18 oxidations to produce aldosterone. This enzyme also generates 18-hydroxycortisol and 18-oxocortisol as metabolites of cortisol, which accumulate significantly in primary aldosteronism. Aldosterone is the principal mineralocorticoid regulating sodium-potassium homeostasis and blood volume, making CYP11B2 central to blood pressure control. The enzyme requires electron transfer via NADPH through a mitochondrial chain comprising ferredoxin reductase (FDXR) and ferredoxins (FDX1/FDX2). Dysregulated CYP11B2 expression and somatic mutations in aldosterone-producing adenomas drive primary aldosteronism, the most common form of secondary hypertension 1. Age-related expansion of aldosterone-producing cell clusters correlates with autonomous aldosterone secretion and cardiovascular risk 2. TRIM2, an E3 ubiquitin ligase, negatively regulates CYP11B2 protein stability; its downregulation in adenomas may contribute to excessive aldosterone synthesis 3. Selective CYP11B2 inhibitors such as levoketoconazole have been developed to suppress aldosterone without affecting cortisol production, offering targeted treatment for resistant hypertension 4. Although gnomAD classifies CYP11B2 as loss-of-function tolerant at the population level (LOEUF=1.01), 131 pathogenic variants in ClinVar demonstrate clinical relevance in disease contexts.