Our finding suggested that myocardial overexpression of Sema3a post-MI might be beneficial in terms of reducing malignant arrhythmias related to increased post-injury sympathetic nerve density, which is obviously associated with the occurrence of ventricular arrhythmia and SCD in animal models or MI patients 10, 28, 29. The gene discussed is SEMA3A; the disease is myocardial infarction.