Primary aldosteronism (PA) is a vastly underdiagnosed (<1 in 500) cause of secondary hypertension in which aldosterone production is inappropriately high relative to suppressed plasma renin levels. This is of major concern as untreated patients are at increased risk for cardiovascular diseases, stroke, and other comorbidities even when compared to matched essential hypertension patients. PA is commonly caused sporadically by aldosterone producing adenomas (APAs) that harbors somatic mutations in aldosterone driver genes. It can account for up to 5 to 10% of hypertensive cases or up to 10 to 20% of resistant hypertensive cases. The current recommended treatment for APAs when only affecting one adrenal is a unilateral adrenalectomy. This has allowed the excised tissue to be extensively studied and characterized. Interestingly APAs have been found to occur with a spectrum of cell morphology and clinical phenotype. This heterogeneity seem to have a genetic basis. KCNJ5 mutant APAs, the most common genotype of APAs, have zona fasciculata (ZF) like cell morphology & secrete hybrid steroids. They commonly are large and frequently occur among young females and Oriental patients. Whereas CACNA1D mutant APAs are smaller, more zona glomerulosa (ZG) like (i.e. more compact than ZF), and more common in Black patients. To note, CACNA1D is also the most common aldosterone driver mutations in aldosterone producing micronodules and elderly patients, followed by aldosterone driver mutations in ATP1A1 and ATP2B3. CTNNB1 mutant APAs that also harbor GNA11/GNAQ mutations have cells that seem to dedifferentiate towards the adrenal-gonadal precursor cell type as they express the LH/HCG receptor ten fold more than other mutant APAs or even CTNNB1 mutant only APAs. This would explain why patients with the double mutations often present at times of high LH/HCG. These distinct genotype specific phenotypes could be used to facilitate screening and diagnosis of PA. For example, hybrid steroid measurements could be used for screening of KCNJ5 mutant APAs; or onset of hypertension in the first trimester (the period of peak HCG secretion), compared to pregnancy associated hypertension in later trimesters, should prompt consideration for a double mutant APA. Moreover, identification of these somatic mutations has already led to potential therapeutic treatments. For example, chemical screens have identified macrolides that selectively inhibit mutant KCNJ5. Thus, histopathology genotype correlation of APAs have provided new opportunities for the screening, diagnosis, management, and treatment of PA. Further elucidations of the cellular mechanisms associated with each correlation will help to identify the pathological and physiological pathways, and thus novel therapeutic targets.