During M1 macrophage polarization, increased H3K18 lactylation significantly induces the expression of homeostatic genes involved in wound healing, such as Arg1.30 Besides, the transition of macrophage from inflammatory to reparatory status is regulated by BCAP-promoting histone lactylation.34 H3K18 lactylation also leads to immunosuppression by inducing METTL3 expression, which mediates m6A modification on JAK1 mRNA in tumor-infiltrating myeloid cells and subsequently phosphorylates STAT3,35 implying that targeting protein lactylation may be also a new approach for tumor therapy. This evidence concerns the gene STAT3 and neoplasm.