In mouse models of esophageal cancer, macrophages recruited by the CCL2-CCR2 axis stimulated immunosuppressive pathways to induce immune evasion by increasing PD-L2 expression and triggering M2 polarization; this suggested the possibility of dual inhibition of the CCRL2-CCR2 axis and the PD-1/PD-L2 signaling pathway and thus, enhanced anti-tumor effects (119). The gene discussed is CCL2; the disease is neoplasm.