These include chemokine-mediated recruitment via CCL20/CCR6, CCL22/CCR4, CCR8, and CXCR3 (95, 96), antigen-driven clonal expansion facilitated by dendritic cell presentation and TGF-β–dependent polarization (96), metabolic reprogramming favoring glycolytic and lipid oxidation pathways to support Treg survival (97, 98), and the contribution of tumor-derived extracellular vesicles that enhance Treg proliferation and confer resistance to apoptosis (99, 100). The gene discussed is CCR4; the disease is neoplasm.