Familial hypercholesterolemia (FH) is an autosomal codominant genetic disorder with an estimated prevalence of 1 in 250 people.1,2 This disorder is caused by pathogenic variants in the LDLR (OMIM 606945), APOB (OMIM 107730), and PCSK9 (OMIM 607786) genes that impair the clearance of low-density lipoproteins (LDLs) from the blood, leading to an increased risk of premature atherosclerotic cardiovascular disease (CVD).3,4,5,6 Despite its prevalence, FH remains underdiagnosed and undertreated.7 The gene discussed is LDLR; the disease is familial hyperaldosteronism.