Qin's research showed that DMY attenuated atherosclerosis through the Nrf2 signalling pathway and induced HUVEC apoptosis.31 Luo's found that DMY protects HUVECs from ox‐LDL‐induced oxidative injury by activating Nrf2/HO‐1 pathway by up‐regulating Akt and ERK1/2.12 Zeng's study showed that DMY reduce foam cell formation via activation of LXRα‐ABCA1/ABCG1 signalling pathway.32 Here, we focus on the PI3k/Akt/FoxO3a pathway, which plays crucial role in promoting survival and function of cardiomyocyte. This evidence concerns the gene AKT1 and atherosclerosis.