Through a series of assays, we found that in MI mice treated with EVs‐miR‐200b‐3p+BCL2L11, the infarction area was widened (Figure 7A), myocardial pathological damage was worsened (Figure 7B), fibrotic area was increased (Figure 7C), TUNEL‐positive apoptotic cells were increased (Figure 7D), inflammatory response (Figure 7E) and oxidative stress (Figure 7F) were promoted, and cardiac function (Figure 7G and 7H) was impaired relative to those treated with EVs‐miR‐200b‐3p+Neg. This evidence concerns the gene BCL2L11 and infarction.