Hence, when the PI3K/Akt/mTOR pathway is altered, in case of over expression, obesity may be developed; if obesity persists as a chronic condition, the excess of free fatty acids in blood due to increased lipolysis, can cause alteration in other non-AT tissues, for example resulting in ectopic lipids in skeletal muscle, decreasing glucose transport and glycogen synthesis, leading to imbalance in glucose metabolism [39,83,86]. The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.