The Low-density lipoprotein receptor (LDLR) gene encodes a protein that is one of the hepatocyte surface receptors that binds apolipoprotein E (APOE) and thus removes lipoprotein particles from the blood. LDLR also plays an important role in cholesterol homeostasis by interacting with apolipoprotein B (APOB) on low-density lipoprotein (LDL) particles (the major cholesterol-carrying lipoprotein in plasma) to bind LDL and transport it into cells by endocytosis, thus maintaining plasma LDL levels ^[1-2]. This process occurs mainly in the liver, which removes approximately 70% of LDL from the circulation, and LDLR regulates plasma cholesterol levels by removing LDL and intermediate-density lipoproteins (IDL) from the plasma. Loss-of-function mutations in the LDLR gene cause familial hypercholesterolemia (FHCL1), a lipoprotein disorder characterized by elevated LDL cholesterol levels. The disease causes excessive deposition of cholesterol in tissues, which subsequently leads to macular tumors, accelerated atherosclerosis, and an increased risk of premature coronary heart disease ^[3-4]. This strain is an Ldlr deletion mouse model that uses gene editing technology to knock out the expression of human LDLR gene homolog in mice with impaired LDLR receptor synthesis, resulting in elevated serum cholesterol levels, which are further exacerbated by feeding on a high-fat diet (HFD), and the formation of aortic plaques. Homozygous Ldlr KO mice are viable and fertile and can be used for studies such as hypercholesterolemia and atherosclerosis. A similar strain includes Ldlr KO (tm) (catalog number: C001278), which was constructed using embryonic stem (ES) cell technology.