APOE and atherosclerosis: We found that EC-iDKO/EC-IP3R1fl/+/ApoE−/− mice displayed a phenotype with aortic atherosclerotic plaques that were larger than that of EC-iDKO/ApoE−/− mice, approximate 60–70% of the size of plaques in ApoE−/− mice, suggesting that endothelial IP3R1 heterozygosity restores atherosclerosis in epsin-deficient mice and that the atheroprotective effect of epsin deletion was mainly resulted from IP3R1 stabilization by prevention of proteasomal degradation (Fig. 7h, i).