FOXP3 and neoplasm: Pharmacologically or genetically disruption of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) activity, which is a histone H3K27 methyltransferase of the polycomb repressor complex 2 (PRC2) in Treg cells, resulted in the loss of FOXP3 expression and conversion to ex-Tregs cells producing high amounts of pro-inflammatory cytokines, such as TNF-α, IFN-γ, and IL-2 in the tumor tissues but not in lymphoid organs.