Wang et al. demonstrated that accumulation of H3K4me3 in the promoter of FOXP3 results in the generation of Tregs, and pharmacological or genetic suppression of the activity of EZH2 on tumor-infiltrating Tregs (TI-Tregs) results in the acquisition of pro-inflammatory functions (Wang et al., 2018a) (Figure 2). The gene discussed is EZH2; the disease is neoplasm.