METTL3 principally functions as an oncogene to promote carcinogenesis in various cancers: METTL3 depletion induced cell differentiation and apoptosis to delay acute myeloid leukemia progression by regulating m6A modification on MYC, BCL2, and PTEN mRNAs (25); high expression of METTL3 correlates with poor clinical outcomes in glioblastoma, and the m6A modification on SRSF transcript added by METTL3 leads to human glioblastoma outgrowth and self-renewal (34). Here, MYC is linked to cancer.