Similarly, exposure to TGF-β1 in the TME promotes the transition of neutrophils from the anti-tumor N1 phenotype to the pro-tumorigenic N2 phenotype [50], albeit by mechanisms that remain unclear, but appear to involve increased reactivities of the neutrophil pro-oxidative enzyme, myeloperoxidase [51] and the arginine-limiting enzyme, arginase 1 [52]. The gene discussed is TGFB1; the disease is neoplasm.