AKT1 and glioblastoma: Due to its higher binding affinity to phosphorylated PDK1 (p-PDK1), AKT3-174aa prefers to interact with activated PDK1, blocking Akt phosphorylation at Thr308 and negatively modulating PI3K/AKT signal intensity to reduce cell proliferation, resulting in the reduction of tumorigenicity and the radiation resistance of GBM [54].