Association between positive remodeling and unstable lesions has been suggested [41,42] and therefore it could be speculated that outward remodeling would be greater in diabetic patients with accelerated atherosclerosis and thus possibly also in the diabetic IGF-II/LDLR-/-ApoB100/100 mice with a more inflammatory vascular phenotype and advanced lesions [20]. This evidence concerns the gene LDLR and atherosclerosis.