CCL22 and cancer: Excessive osteoclasts promote bone resorption, ultimately facilitating the formation of PMN.45 These macrophages interact with soluble mediators derived from primary tumors and gradually transform into phenotypes that promote immunosuppression and angiogenesis.46,47 TAMs facilitate the recruitment of Treg cells to the PMN through the secretion of CCL22.48 Macrophages display functional plasticity in response to local microenvironmental cues and contribute to cancer-related inflammation, extracellular matrix (ECM) remodeling, immune evasion, and ultimately cancer metastasis.