Accumulating evidence has confirmed that EZH2 is frequently mutated and abnormally overexpressed in various malignant tumors including prostate cancer,415,416 ovarian cancer,417 endometrial carcinoma,418 breast cancer,419 melanoma as well as hematological malignancies,420 such as NHL, B-cell lymphoma, and T-cell ALL.421–424 It promotes tumorigenesis mainly through three mechanisms: PRC2-dependent H3K27 methylation, PRC2-dependent non-histone protein methylation, and PRC2-independent coactivator of transcriptional factors. This evidence concerns the gene EZH2 and cancer.