AKT1 and glioblastoma: Taken together, all of our results demonstrated that POU2F2 directly promoted the transcription of PDPK1, and then POU2F2 interacted with AKT, activated PI3K/AKT/mTOR pathway to increase the expression of GLUT1, HK2, and PKM2, leaded metabolic shift towards aerobic glycolysis, and promoted GBM progression (Fig. 8).