In most cancers, macrophages are enriched by infiltrating MDMs that are recruited from the periphery in response to signals from the TME (e.g., CCL2, CCL9, CSF-1, VEGF, and TGF-b), and their in situ phenotype is shaped by a combination of organ- and tumor-derived signals [2, 47]. The gene discussed is CCL2; the disease is cancer.