eNOS‐deficient(−/−) mice showed significantly larger infarct size and more neutrophil accumulation in myocardial ischaemia‐reperfusion injury,31 overexpression of eNOS attenuated myocardial reperfusion injury,32 implying increasing eNOS pathway activation could constitute a promising strategy in MI. The gene discussed is NOS3; the disease is myocardial infarction.