Depletion of METTL3 or METTL14 in tumor cells increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-γ, CXCL9, and CXCL10 in the TME, thereby enhancing the response to anti-PD-1 treatment in mismatch-repair-proficient or microsatellite instability-low CRC tumors [70]. This evidence concerns the gene PDCD1 and neoplasm.