Although the primary function of EZH2 is gene silencing through the methylation of H3K27, most evidence shows that EZH2 functions independently of H3K27me3 in various cancers; for instance, in some cancers EZH2 was shown to interact with β-catenin and promote its nuclear accumulation and activation [7], to form the β-catenin/T-cell factor (TCF) transcriptional activator, which up-regulates a number of target genes such as survivin, c-Myc and VEGF [8]. Here, MYC is linked to cancer.