Because a previous study demonstrated that the overexpression of RIOK2 promoted proliferation and tumorigenesis, whereas the silencing of RIOK2 inhibited the proliferation and survival of glioma cells and prolonged the survival time of glioma-bearing mice25, these findings suggested that BYSL may function by regulating RIOK2 to promote glioma cell growth. The gene discussed is RIOK2; the disease is central nervous system cancer.