Detection of inflammatory response (Figure 6A and 6B), oxidative stress (Figure 6C through 6E), and cardiac function (Figure 6F through 6H) manifested that sh‐BCL2L11 promoted the role of EVs in decreasing IL‐1β and IL‐18 levels, suppressing malondialdehyde and ROS contents, and improving SOD activity, as well as reducing LVEDD and LVESD and increasing LVEF and LVFS; while the effect of EVs was reversed by BCL2L11 upregulation in MI mice. This evidence concerns the gene BCL2L11 and myocardial infarction.