In addition, Increased physical activity after myocardial infarction promotes BDNF expression in the hypothalamus, and through BDNF binding to pro-myosin receptor kinase B activates ERK1/2 (the extracellular signal-regulated kinase 1/2) and AKT pathways, promoting macrophage survival (36). This evidence concerns the gene AKT1 and myocardial infarction.