Tumor production of CXCL9 and CXCL10, which are Th1-type chemokines, can be repressed by either enhancer of zeste homolog 2 (EZH2, a core of the PRC2 complex)-mediated histone H3 lysine 27 trimethylation or DNA methyltransferase 1 (DNMT1)-induced DNA methylation, subsequently resulting in less recruitment of IFN-γ-producing immune cells [110]. The gene discussed is CXCL10; the disease is neoplasm.