The presence in the TME of cytokines or immunosuppressive molecules such as transforming growth factor beta (TGF-β) or interleukin 10 (IL-10) can favor the polarization of tumor-associated neutrophils (TANs) towards a protumor phenotype (N2), while the presence of granulocyte colony-stimulating factor (G-CSF) can promote the development of TANs with antitumor activity (N1) [105]. The gene discussed is IL10; the disease is neoplasm.