The molecular basis of increased levels of LDL-C in FH usually derives from genetic variants in the LDLR, leading to a reduced number or activity of LDL receptors and ultimately culminating in diminished hepatic clearance of LDL particles from the blood.1 Other established molecular mechanisms resulting from variants in the APOB or gain-of-function variants in PCSK9 also lead to hypercholesterolemia due to impaired hepatic uptake of circulating LDL. Here, LDLR is linked to familial hyperaldosteronism.