AKT1 and Hyperglycemia: These invading cells and cardiomyocytes produce proinflammatory cytokines such as interleukin (IL)-1, IL-18, and the tumor necrosis factor (TNF).42 These proinflammatory cytokines not only stimulate the expression of CAMs as a positive feedback mechanism, but also have direct and indirect cardiodepressive effects such as apoptosis via the intracellular serine-threonine kinase Akt pathway and modulation of cardiac function.43 Hyperglycemia worsens the mitochondrial generation of ROS and glucose oxidation, thereby causing DNA damage and contributing to accelerated apoptosis.8