Familial hypercholesterolemia (FH), with an autosomal semi-dominant inheritance pattern, is due to a monogenic defect in LDL receptor (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9), or apolipoprotein E (APOE) genes, which encode proteins involved in cholesterol metabolism [1,2]. This evidence concerns the gene APOB and familial hypercholesterolemia.