Multiple studies support the fact that ROS overproduction suppresses ERK1/2 and AKT signaling and eventually leads to cell death [30, 31], suggesting that augmented ERK1/2 and AKT signaling partially affects the rescue process mediated by MHY-1684 in hyperglycemia-induced diabetic cardiomyopathy. This evidence concerns the gene AKT1 and Hyperglycemia.