Previous studies have demonstrated that the underlying mechanisms of the cardioprotective effects of melatonin in MI are related to its abilities to inhibit the inflammatory response, decrease oxidative stress, maintain mitochondrial function, reduce cardiomyocyte apoptosis, and regulate receptor or nonreceptor signaling pathways (such as the MAPK/ERK, AMPK, PI3K/Akt, SAFE, and Notch pathways) [45–47]. The gene discussed is AKT1; the disease is myocardial infarction.