Evidence of activation of effector pathways of HK2-linked unscheduled glycolysis in peripheral insulin resistance has been reported: in the skeletal muscle, mitochondrial dysfunction, increased ROS formation, hexosamine pathway, MG-derived AGEs, and increased Mondo A/Mlx signaling have been found in insulin resistance (149–152) and in adipose tissue, mitochondrial dysfunction, increased ROS formation, increased PKC activity, dicarbonyl stress, and increased Mondo A/Mlx signaling (153–156) (Table 3). The gene discussed is MLX; the disease is Insulin resistance.