Given that like APOE deficiency, ε2 homozygosity is also associated with an increased risk of type III hyperlipoproteinemia in humans [36], together with the fact that knock-in mice carrying the human APOE E2 allele in place of the mouse Apoe gene cause type III hyperlipoproteinemia and spontaneous atherosclerosis in mice [39], Apoe KO mice can be a model mimicking ε2/ε2 carriers. This evidence concerns the gene APOE and hyperlipoproteinemia type 3.