N2-type neutrophils in tumor tissues stimulate Th17 proliferation and differentiation through CCL-20, IL-23 secretion and inhibition of TNF-α production, which in turn strengthens the immunosuppressive effects of Th17 and inhibit antitumor effects of CD4+ Th1 to negatively regulate functional homeostasis to tumor onset (14, 84–86). The gene discussed is CCL20; the disease is neoplasm.