AKT1 and glioblastoma: In one subset, Faury et al. hypothesized that Akt-mediated phosphorylation of YBX-1 contributes to gliomagenesis in pediatric glioblastoma by attenuating the translational repression of many pro-mRNAs by YBX-1, increasing the level of epidermal growth factor receptor, and interfering with the function of p53, A second subset, which is not associated with activation of Akt and Ras pathways, and which may originate from astrocyte progenitor cells [96].