One explanation is the high levels of the transcription factor FoxG1 expressed in GBM cells, which interacts with FoxO3, inhibiting the capacity of TGF-β to induce p21Cip1 expression [65], responsible for the inhibition of the activity of cyclin-dependent kinase (CDK)2 and CDK4 complexes and promoting cell cycle G1 phase arrest [66]. This evidence concerns the gene TGFB1 and glioblastoma.