Additionally, Mettl3- or Mettl14-deficient tumors upregulated cytotoxic tumor-infiltrating CD8+ T cells and increased the production of IFN-γ, Cxcl9 and Cxcl10 in the TIME of CRC in vivo, thereby enhancing the response to anti-PD-1 treatment (127). This evidence concerns the gene METTL3 and neoplasm.