Specifically, the recruitment of immune‐suppressive cells such as CCR2+ tumor‐associated macrophages (TAMs) or MDSCs to the TME by CCL2 weakens the body's anti‐tumor immune response, creating an immune‐suppressive microenvironment that fosters tumor progression.[41, 63, 64] Therefore, CCL2 may be a promising target for BC treatment. This evidence concerns the gene CCR2 and neoplasm.