In line with our findings, previous evidence has shown that oxLDL and lipid peroxidation products trigger ER stress and the production of UPR, characterized by GRP78 localization in ApoE−/− mouse vascular cells and atherosclerotic lesions [5, 6, 35, 36], and in the plasma of patients with metabolic disorders [37]. This evidence concerns the gene APOE and metabolic disease.