At the tumor site, similarly to macrophages, tumor-associated neutrophils (TAN) possess two main polarized statuses that can switch into one another and play opposite roles on tumor progression: the so-called N1 with antitumoral phenotype induced mainly by IFN-β stimulation and the tumor-promoting phenotype N2 elicited by TGF-β, G-CSF, and IL-6 [22]. The gene discussed is IL6; the disease is neoplasm.