In glioblastoma (GBM), exosomal miR-1238 mediates the acquired resistance of GBM cells to TMZ by directly targeting the CAV1/EGFR pathway and affecting the activation of the PI3K-AKT-mTOR signaling pathway[47], while exosomal circUHRF1 was found to induce natural killer cell exhaustion and contribute to anti-PD1 therapy resistance[57]. Here, AKT1 is linked to glioblastoma.