No matter whether DMY functions in diabetes by improving glucose and lipid homeostasis in the liver, adipose tissue, and skeletal muscle, or assists in reducing NAFLD through AMPK/PGCl-α/ERR-α or facilitated tumor cell apoptosis through AMPK/GSK3/SOX2 and regulated the AMPK/GLUT4 signaling pathway in the treatment of diabetic encephalopathy, AMPK has been recognized as the most upstream of these cascades, making AMPK is a key target for DMY in the treatment of these diseases. This evidence concerns the gene SOX2 and diabetic encephalopathy.