The present study found that ACh-induced endothelial dysfunction in ApoE KO mice was ameliorated by Tudca, the ER stress inhibitor (Fig. 3C), and Tunicamycin, the ER stress inducer, directly impaired endothelium-dependent vasodilation in the WT and ApoE KO-EX mice, but not in ApoE KO mice (Fig. 3A, B). Here, APOE is linked to endothelial dysfunction.