The literature describes a few major defects as being the cause for FH: 87% of the patients have a pathogenic variant in the LDL-receptor (LDL-R) gene; 10% in the gene for its ligand, apolipoprotein B 100 (ApoB-100); less than 5% have a defect in the subtilisin-kexin type 9 proprotein convertase gene (PCSK9); and an extremely rare (<1%) cause can be a pathogenic variant in the LDL-R adaptor protein 1 (LDLRAP1) gene [6,7]. The gene discussed is LDLR; the disease is familial hyperaldosteronism.