Together with our previously report that CUL4B attenuated irradiation and oxidative stress-induced senescence in normal human fibroblasts (NHFS) and osteosarcoma cell lines U2OS cells (42), we believe that impeding cellular senescence is an important mechanism through which CUL4B promotes TMZ resistance in GBMs. The gene discussed is CUL4B; the disease is osteosarcoma.