The genetically modified mouse models ApoE−/− (King 2010; Canizzo 2012) [107,108] and LDL−/− [109,110] also failed as pure diet-induced diabetic atherosclerosis models, because they have exhibited inconsistent effects on blood glucose or insulin levels or on the development of insulin resistance, and the variable increment of plaques would mainly be related to hyperlipidemia rather than to alterations in glucose metabolism. The gene discussed is APOE; the disease is hyperlipidemia.