Thus, we propose a model to explain SOX4’s action in GBM cell lines: SOX4 could down-regulate Akt, which might result in increased stability of p53, as shown by increased p53 protein expression in SOX4 overexpressed GBM cell lines and induced p21 signal which leading to G0/G1 cell cycle arrest. Here, AKT1 is linked to glioblastoma.