Our discoveries illustrated that CCL2 affects the activation of MAPKs in M‐MDSCs and that CCL2 stimulated M‐MDSC‐modulated impedance of T lymphocytes raising the question of whether M‐MDSCs, CCL2, and M‐MDSC/CCL2‐regulated suppression of T lymphocytes in tumor microenvironment might be significant factors to consider when identifying the reason why current ICP therapies might not take effect on all tumor‐bearing patients. The gene discussed is CCL2; the disease is neoplasm.