Approximately 95% of these cases are sporadic, with the remaining 5% caused by a pathogenic variant in genes that result in an increase in the transcription and expression of CYP11B2, which is responsible for aldosterone synthesis (familial hyperaldosteronism (FH) types II, III, and IV) or a fusion of the CYP11B2 and CYP11B1 genes, which is responsible for FH-I or glucocorticoid-remediable PA (GRA) (2). Here, CYP11B1 is linked to familial hyperaldosteronism.