We demonstrated that high METTL3 expression in CRC cells induced the m6A-BHLHE41-CXCL1 axis to promote the infiltration of myeloid-derived suppressor cells (MDSCs) in the CRC microenvironment, and that the loss of METTL3 in CRC compromised its ability to drive MDSC accumulation and suppressive potency, resulting in enhanced anti-tumor immune responses and diminished CRC growth [77]. The gene discussed is METTL3; the disease is neoplasm.