Patients with heterozygous familial hypercholesterolemia (HeFH) are characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and elevated risk of atherosclerotic cardiovascular disease (ASCVD), most commonly resulting from autosomal dominant mutations in genes of the LDL receptor pathway (e.g., the LDLR, APOB, and PCSK9 genes) [1, 2]. The gene discussed is LDLR; the disease is familial hypercholesterolemia.