Globally, our findings suggest that FC85 actively enhances downstream p53 signalling and that a combination strategy aimed at inhibiting PI3K/AKT/mTOR signalling and activating p53 signalling is potentially effective in GBM and in its CSC subpopulation, where TP53 mutations are rare, and the downstream p53 signalling is intact. The gene discussed is AKT1; the disease is glioblastoma.