Given that RIOK loss upregulates p53 levels, we tested whether knockdown of RIO kinases could potentiate the response of GBM cells to treatments with DNA-damaging agents such as doxorubicin, which cooperates with p53 to provoke apoptosis, [57], [58] and temozolomide, which is a DNA alkylator used to treat GBM. The gene discussed is TP53; the disease is glioblastoma.