For example, MCT1 tri‐methylation mediated by the methyltransferase SETDB1 sustains MCT1 stabilization and in turn promotes tumor glycolysis and M2‐like polarization of TAMs in colorectal cancer, which contributes to tumor immunosuppression.[15] These studies indicate that abnormal methylation exacerbates the immunosuppressive TME by regulating tumor cell‐macrophage intercellular crosstalk, suggesting that targeting methylation or methyltransferases in the TME may be a strategy for tumor treatment. The gene discussed is SETDB1; the disease is neoplasm.