Xenograft studies revealed that depletion of either SVIL, MLL1, or YTHDF2 profoundly antagonizes tumorigenesis of LNZ308-p53(G245D) glioma cells, suggesting a critical oncogenic role of the mutant p53/SVIL/MLL1 complex by activating YTHDF2 to promote tumorigenesis in vivo (Fig. 6a). The gene discussed is KMT2A; the disease is central nervous system cancer.