Contrary to other mouse models of atherosclerosis, low-density lipoprotein receptor (LDLR)-deficient mice phenocopy human patients with familial hypocholesteremia [28], show a rather human-like pro-atherogenic lipid profile (high low-density lipoprotein (LDL)) and due to the presence of functional apolipoprotein E (APOE), the development of concomitant inflammation in atherosclerosis is not compromised (unlike in APOE-deficient mice) [29,30]. This evidence concerns the gene LDLR and atherosclerosis.