TAMs can be proliferative, which could provide a compensatory mechanism when monocyte recruitment is impaired.48 Recent work has demonstrated that in lung metastatic sites, TAMs are derived from both CCR2‐dependent monocytes and resident interstitial Mφs, each promoting tumor growth and metastatic spreading, respectively.104 Additional work is needed to better understand the relative contributions of monocytes and resident Mφ populations to TAM accumulation and phenotype across different tumor types. This evidence concerns the gene CCR2 and neoplasm.