An investigation by Huaizhu Wu et al. was done to determine the role of CD11c in hypercholesterolemia and atherogenic lesion and it was found that on APOE double deficiency hypercholesteromic mice the expression of CD11c was increased and the number of circulating monocytes were increased compared to wild type APOE double deficiency normal fed mice. This evidence concerns the gene APOE and familial hypercholesterolemia.