For instance, Xiong et al. demonstrated that in tumor-infiltrating myeloid cells, lactate induces METTL3 expression via H3K18 lactylation (Galle et al., 2022), and this METTL3-mediated m6A modification promotes immunosuppression via JAK/STAT signaling (Xiong et al., 2022) connection suggests a potential mechanism whereby lactate-driven METTL3 induction and subsequent m6A deposition may contribute to the dysregulated immune response and immunosuppression observed in septic patients. This evidence concerns the gene METTL3 and neoplasm.