Granot et al. found that in a mouse 4T1 BC model, the accumulation of TENs (neutrophils induced by the primary tumor) in the lung during premetastatic stages limited metastatic progression via neutrophil-derived H2O2, which provided antitumor functions, and tumor cell-derived CCL2 was responsible for the accumulation of TENs [76]. Here, CCL2 is linked to neoplasm.