Because the hyper-activation of the PI3K/AKT/mTOR pathway and the inactivation of wild-type p53 by MDM2 over-expression are frequent molecular events in highly proliferative tumours, and the aforementioned pathways are directly related29, a combined therapy with an inhibitor of AKT/mTOR pathway and a compound able to inhibit the MDM2/p53 interaction may represent a valuable approach in GBM. The gene discussed is AKT1; the disease is neoplasm.