In the microenvironment of myocardial infarction, M1 macrophages can inhibit the ability of endothelial cells to generate blood vessels, aggravate the degree of myocardial infarction injury, and hinder cardiac repair, all of which are attributed to the pro-inflammatory M1-Exos released by M1 macrophages and the miR-155 they contain which downregulate the RAC1-PAK1/2 and Sirt1/AMPKα-eNOS pathways (150). This evidence concerns the gene RAC1 and myocardial infarction.