We also identify the upregulation of platelet-specific genes, for instance, GP1BB, GP1BA, ITGA2B, TREML1, in PBMCs from the MI patients (Figure 7C), which may in part be attributed to the formation of leukocyte-platelet aggregates (39, 40) or platelet-derived extracellular vesicles (PEV) (53). This evidence concerns the gene ITGA2B and myocardial infarction.