To study pathomechanisms of atherosclerosis, hypercholesterolemic, apolipoprotein E (ApoE)-deficient mice are often used as a model because these mice reproduce major features of atherosclerotic vascular disease such as hypercholesterolemia-induced atherosclerotic lesion formation in the vascular system with increasing age (4–8). This evidence concerns the gene APOE and familial hypercholesterolemia.