The importance of macrophage-derived apoE in protection from atherosclerosis is documented in bone marrow transplantation studies showing that the reconstitution of macrophage apoE expression was sufficient to prevent atherosclerosis in hypercholesterolemic ApoE−/− mice (39, 40, 41), whereas the transplantation of apoE-deficient bone marrow was found to exacerbate atherosclerosis in Ldlr−/− and C57BL/6 WT mice with physiologically regulated apoE expression in the liver (42, 43). This evidence concerns the gene LDLR and atherosclerosis.