Potential therapeutic methods of correcting disease-causing mutations or of knocking out specific genes as approaches for the prevention of CVDs have gained substantial attention using genome editing techniques.7-9 Videlicet, gain-of-function mutations in the pro-protein convertase subtilisin-like kexin type 9 (PCSK9) gene, which is a major regulator of low-density lipoprotein (LDL) receptor levels and LDL-cholesterol concentrations, have been reported to increase LDL-C levels, leading to an increased risk of hypercholesterolemia and coronary heart disease (CHD). This evidence concerns the gene LDLR and familial hypercholesterolemia.