Our previous studies have provided firm evidence that KDM3A is implicated in diabetic vascular remodelling and diabetic cardiomyopathy as well as myocardial ischaemia‐reperfusion injury by regulating key signalling pathways that are involved in inflammation, apoptosis and oxidative stress.15, 17 In addition, Zhang and colleagues also reported that KDM3A participated in left ventricular hypertrophy and myocardial fibrosis in response to pressure overload.18 In the light of these considerations, we speculated that KDM3A may play a central role in the regulatory network of AMI. The gene discussed is KDM3A; the disease is Myocardial fibrosis.