Known as a wide-ranging oncogenic determinant, c-MYC was found to be upregulated by METTL3 via m6A/DLGAP1-AS2/YTHDF1 in non-small cell lung cancer (NSCLC)220 and m6A/YTHDF/APC/β-catenin in ESCA, further advancing glycolytic metabolism.221 HIF-1α is responsible for hypoxia conditions in tumor environment, which form mutual feedback with tumor growth. This evidence concerns the gene METTL3 and neoplasm.