AKT1 and glioma: VM formation occurs mainly through glioma stem cells and the transforming growth factor beta (TGFβ), vascular endothelial growth factor receptor 2 (VEGFR-2)/fetal liver kinase 1 (FLK-1), vascular endothelial cadherin (VE-cadherin), receptor tyrosine kinase (RTK)/phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), and MMP-laminin5γ2 chain pathways [33, 34].