AKT1 and glioma: The process of neoangiogenesis in gliomas may have a dual mechanism—dependent on hypoxia or excessive activity of pathways such as the PI3K/Akt signaling pathway (phosphatidyl-inositol 3-kinase-serine/threonine kinase Akt) or RAS/MAPK/ERK (rat sarcoma protooncogene/mitogen-activated protein kinase/extracellular signal-regulated kinase) via mutation or constitutive activation of their components [17].