In conclusion, MI-associated EVs can deliver miR-208b to HUVECs, and the enrichment of miR-208b may suppress cell viability and migration, as well as promote cell apoptosis by regulating apoptosis-related genes (Bcl2 and Bax) and the FAK/MAPK1/Raf-1 pathway. This evidence concerns the gene BCL2 and myocardial infarction.