Fridlender’s group was able to inhibit the N2 response in tumors and polarize them by shifting the balance using TGFβ blockade, which increased neutrophil-attracting chemokines, resulting in an influx of the N1 subtype CD11b( +)/Ly6G( +) TANs with hypersegmented nuclei (polymorphonuclear cells) that were more cytotoxic to tumor cells, and expressed higher levels of the pro-inflammatory cytokines [48]. Here, TGFB1 is linked to neoplasm.