AKT is essential for the insulin-mediated effect on metabolism as it starts by the stimulation of glycogen synthesis via Akt-mediated inhibition of glycogen synthase kinase-3, and glycogen synthase [31], while VEGF overexpression leads to an increase in brown adipose tissue (BAT) thermogenesis and also promotes a “BAT-like” phenotype in white adipose tissue depots which may protect against diet-induced obesity and insulin resistance [9]. This evidence concerns the gene AKT1 and Insulin resistance.