Several experimental studies with apoE‐/‐ mice found that PSRC1 overexpression could inhibit the accumulation of cholesteryl ester in foam cells and alleviate the development of atherosclerosis by raising plasma HDL‐c levels and enhancing HDL function,[49] while PSRC1 deficiency could increase trimethylamine N‐oxide (TMAO) production through manipulating gut microbiota[50] and impair cholesterol transport by activation of sulfotransferase 2B1b,[51] thereby accelerating atherosclerosis, which supported our findings that PSRC1 overexpression had therapeutic potential for CAD. Here, APOE is linked to atherosclerosis.