Recent studies have shown that active glycolysis in tumor cells depletes extracellular glucose and restricts its availability to host cells, leading to impairment of T cell glycolytic metabolism, while the expression of PD-L1 by tumor cells promotes constitutive activation of the Akt/mTOR pathway and treatment with anti-PD-L1 antibodies attenuates both glycolysis and phosphorylation of Akt [13, 14]. This evidence concerns the gene AKT1 and neoplasm.