FOXP3 and neoplasm: MDSCs dwindle adaptive immune responses via the induction of FOXP3+ regulatory T cells (Treg), by the polarization of T cells toward a tumor-promoting type 2 phenotype, by the inhibition of T-cell function and proliferation through production of ARG1 and inducible nitric oxide (NO) synthase 2 (iNOS2) or, in an l-arginine-independent manner, via reactive oxygen species (ROS) and TGF-β production, cysteine depletion, and L-selectin (CD62L) downregulation [64,65].