Among those, the most extensively investigated is the ApoE KO that lacks ApoE, a glycoprotein ligand for receptors that eliminates chylomicron remnants and very low-density lipoproteins (VLDLs), which exhibits spontaneous hypercholesterolemia and the formation of atherosclerotic lesions in vessels [86,87]. The gene discussed is APOE; the disease is familial hypercholesterolemia.