It is possible that the myocardial Sema3a overexpression in a post-MI model might help to restore the myocardial Sema3a level to the pre-MI status, thus, be beneficial on inhibiting cardiac nerve sprouting and attenuating sympathetic hyper-innervation post-MI and result in reduced inducibility of malignant arrhythmias during EPS in our model, whereas the general myocardial overexpression of Sema3a in the non-MI transgenic mice model ‘resulted in’ too much myocardial Sema3a which was linked with the observed catecholamine supersensitivity and prolongation of the action potential duration. This evidence concerns the gene SEMA3A and myocardial infarction.