In mismatch‐repair‐proficient or microsatellite instability‐low (pMMR‐MSI‐L) tumors with low mutation burden, which constitutes about 85% of CRC, depletion of METTL3/14 could enhance ICB responses through increasing infiltration of cytotoxic CD8 + T cells and promoting secretion of IFN-γ, CXCL9, and CXCL10 in TME in vivo [135]. This evidence concerns the gene CXCL9 and colorectal carcinoma.