Some study suggested that HIF-2α expression was significantly induced by in heart.28 Other study showed that HIF-1α and HIF-2α protein accumulates after myocardial infarction.29 The silencing of HIF-2 but not HIF-1 prevented the activation of arginase II by hypoxia.30 Thereby, we hold that arginase is a target of HIF-2α. Here, EPAS1 is linked to myocardial infarction.