Complement proteins, cytokines, and chemokines like C3a, C5a, GM-CSF, CXCR1/2 agonists, IL-8, IL-17, and IL-1β within the TME (the specific cytokine/chemokine composition varies between tumors) can recruit neutrophils and reprogram them towards pro-tumor (N2 or PMN-derived suppressor cells (PMN-MDSCs)) or antitumor (N1) functionalities [227,228]. The gene discussed is CSF2; the disease is neoplasm.