Initially, our experimental data highlighted that injection of MSCs‐EVs into the heart of mice with MI could attenuate the infarction area and pathological injury, reduce collagen volume fraction value and apoptotic rate, restore cardiac function (decreased heart rate, LVEDD, LVESD, and left ventricular end‐diastolic pressure, and increased LVEF, LVFS, and LVSP), and suppress oxidative stress (reduced malondialdehyde and ROS and enhanced SOD activity). The gene discussed is SOD1; the disease is myocardial infarction.