In glioblastoma, PTEN deficiency increases PI3K/AKT pathway activation, which in turn enhances the biologenesis of EVs enriched with PD-L1 (PD-L1 is expressed on tumor cells and inhibits T-cells function by binding to PD-L1, Leading to apoptosis or functional exhaustion of T cells) [72, 73]. This evidence concerns the gene AKT1 and neoplasm.