Pollard and colleagues found that in the MMTV–PyMT mouse model of breast cancer, Gr1+ inflammatory monocytes expressing CCR2 (receptor for CCL2) were recruited to the premetastatic lung through CCL2 secreted by tumor and stromal cells and differentiated into tumor-associated macrophages (TAM) to promote the subsequent growth of metastatic cells. This evidence concerns the gene CCL2 and neoplasm.