The gain-of-function role for mutant EZH2 in cancer is always resulted by the other chromatin regulators’ loss-of-function mutations which can normally antagonize EZH2 activity, such as the ubiquitously transcribed tetratricopeptide repeat gene on X chromosome (UTX) (van Haaften et al., 2009; Gui et al., 2011). This evidence concerns the gene KDM6A and cancer.