AKT1 and glioblastoma: Therefore, the GBM cells were cocultured with the M2-CM, and we found that M2-CM upregulated p-PI3K, p-Akt, and Nrf2 to activate the PI3K/Akt/Nrf2 pathway, which were reversed by silencing VEGF, suggesting that M2-CM activated this pathway in a VEGF-dependent manner.