Individuals suffering from familial hypercholesterolemia (FH), an autosomalco-dominant disorder caused by mutations in the LDL receptor, are atparticular risk of developing premature atherosclerotic cardiovasculardisease (ASCVD) compared to normolipidemic individuals, as they often failto adequately respond to lipid-lowering medications.4, –6 Inaddition to LDL-C, Lp(a) is frequently elevated in FH, despite the lack ofclear evidence of a crucial role of the LDL receptor in Lp(a) plasmaclearance. The gene discussed is LDLR; the disease is familial hypercholesterolemia.