In parallel, tumor-conditioned myeloid cells undergo epitranscriptomic reprogramming: lactate accumulation in the TME induces METTL3 via protein lactylation, which enhances m6A-JAK1–STAT3 signaling in tumor-infiltrating myeloid cells and reinforces immunosuppressive transcriptional programs. The gene discussed is METTL3; the disease is neoplasm.