AKT1 and glioblastoma: Downregulation of urokinase-type plasminogen activator/urokinase-type plasminogen activator receptor (uPA/uPAR), a multifunctional system playing a critical role in GBM invasion, inhibited the cleavage of the Notch receptor, thus inhibiting Notch signaling-induced AKT, NF-κB, and extracellular signal-regulated kinases (ERK) pathways[75].