Thus, all recipient mice received ApoE+/+–bone marrow cells to mitigate the previously described effects of total ablation of this apolipoprotein on both classical/proinflammatory (M1) and alternative/anti-inflammatory (M2) polarization (12) and to provide them with a physiologically important source of APOE to aid normalization of plasma cholesterol levels and of the lipoprotein profile in this otherwise extreme hyperlipidemic mouse model of human atherosclerosis (12, 20). This evidence concerns the gene APOE and atherosclerosis.