Mice deficient in the LDL receptor ligand, ApoE (ApoE−/−) involved in uptake of LDL, fed a HFHC diet, exhibit an atherosclerosis phenotype with high blood oxLDL levels [21]; along the lines of the concept presented herein, these animals also exhibit laminar deposits in BM, as seen in AMD [24]. This evidence concerns the gene LDLR and atherosclerosis.