Another intriguing study has demonstrated that the crosstalk between T cells and neutrophils promotes metastatic breast cancer [49]; tumor-derived IL-1β elicits IL-17-producing γδ T cells, which drives G-CSF-dependent expansion and the functional polarization of neutrophils toward a CD8+ T cell-suppressive phenotype, thereby promoting subsequent metastasis formation in distal organs. Here, CSF3 is linked to neoplasm.