Therefore, we speculated that LXFG may be regulating expression of effector P-Bad via the NGF/TrKA/PI3K/AKT signaling pathway, causing a balance between survival, regeneration, and apoptosis of sympathetic neurons, thereby attenuating sympathetic remodeling and reducing occurrence of arrhythmia in rats following MI. This evidence concerns the gene AKT1 and myocardial infarction.