These findings along with the in vitro findings convincingly indicated that the JNK activator anisomycin nullified melatonin-induced cardioprotection against high-glucose/high-fat-hypoxia-induced cardiac biochemical and functional deficits, validating the role for the JNK pathway in melatonin-offered benefit against post-MI in diabetes. The gene discussed is MAPK8; the disease is myocardial infarction.