AKT1 and glioblastoma: To date, several studies have demonstrated that RIOK2 is overexpressed in GBM tumor cells relative to normal brain cells [13,14,15], and RIOK2 loss causes a reduction in Akt signaling and provokes p53-dependent apoptosis, cell cycle exit, and chemosensitivity through the RpL11-dependent ribosomal stress checkpoint [13], which in turn suggests that RIOK2 is engaged in tumorigenic activity in GBM, can be a potential target for anti-GBM.