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. This evidence concerns the gene SEMA3A and Schnyder corneal dystrophy.