Under normal conditions, AMPK remains dephosphorylated and inactive state; when energy is shortage, such as obesity and MS, AMPK is phosphorylated at the site of Thr172 and actived, which directly phosphorylates the Thr2446 site of mTOR, inhibits Akt-mediated phosphorylation of Ser2448, indirectly inhibits mTOR activity, thus activates autophagy. This evidence concerns the gene AKT1 and obesity due to melanocortin 4 receptor deficiency.