However, it has to be considered that, unlike our murine disease model eliciting only atherogenic remodeling and initial atherosclerotic lesions, these studies investigated more advanced stages of atherosclerosis in atheroprone mouse strains lacking the LDL receptor or the apolipoprotein E. While these genetic mouse models may better mimic the complete picture of human atherosclerosis, the lifelong defect in lipid homeostasis resulting in excessive hypercholesterolemia might also be a confounding factor29. This evidence concerns the gene LDLR and familial hypercholesterolemia.