Based on these results, we employed the special inhibitor of JAK2 in this I/R model, and then re-evaluated the heart Hemodynamic parameters, myocardial infarct size, proinflammatory cytokines and myocardial cell apoptosis to investigate the role of JAK2 activation in the myocardial protection of EDT. The gene discussed is JAK2; the disease is myocardial infarction.