The expression of P-AKT and P-mTOR were both increased after treated with EXO from glioma cells under hypoxic condition and miR-25-3p overexpression in HMC3 and PBMCs-derived macrophage but abolished by miR-25-3p inhibitor and LY294002, an inhibitor of the PI3K-AKT signaling pathway (Fig. 4B-F). This evidence concerns the gene AKT1 and central nervous system cancer.