MSCs modified to overexpress endothelial nitric oxide synthase (eNOS) were more potent than control MSCs and eNOS adenoviral vector in reducing the myocardial infarct size (4 and 2-fold increase, respectively), corrected hemodynamic parameters and increased the capillary density by increasing nitric oxide production (Chen L. et al., 2017). Here, NOS3 is linked to myocardial infarction.