While there is sparse evidence in the literature pointing at a perhaps underappreciated involvement of TGF-β-activated PI3K/AKT and MAPK signaling in the regulation of EMT-like programs in GBM [174, 202–205], further experimental work is required to precisely define how these pathways promote the emergence of mesenchymal phenotypes in glioma cells. Here, AKT1 is linked to glioblastoma.