In CRC, lactylation modification of METTL3 in tumor‐infiltrating myeloid cells promotes m6A‐dependent JAK–STAT3 axis activation and inhibits tumor immunity.[25] In gastric cancer, lactylation modification of METTL16 promotes FDX1 m6A‐dependent mRNA stability and promotes cuproptosis.[26] VIRMA is a methyltransferase that acts as an m6A writer and promotes tumorigenesis in various cancers in an m6A‐dependent manner;[27] however, its underlying mechanism in CRLM remains unclear. The gene discussed is STAT3; the disease is neoplasm.