AKT1 and glioblastoma: Furthermore, our recent studies demonstrated that PTEN deletion/mutation and metabolic alteration in GSC/GBM cells can activate the SRC/AKT-YAP1 and YAP1/STAT3 pathways to upregulate the expression of chemokines (e.g., lysyl oxidase, CCL2, and CCL7), triggering macrophage migration and promoting tumor progression (13, 14).