AKT1 and glioblastoma: Erlotinib upregulates promyelocytic leukemia (PML) protein, which is a negative regulator of AKT-mTOR signaling, to promote resistance to erlotinib, and treatment with a PML inhibitor chemosensitizes glioblastoma cells to erlotinib and an mTOR inhibitor, suggesting the clinical relevance of the combination of PML-targeting drugs and erlotinib [51].