Interestingly, EZH2 overexpression in NKTL was found not to be associated with H3K27 trimethylation [35], and ectopic expression of an EZH2 mutant lacking HMTase activity in NKTL cell lines rescued the tumor growth inhibition resulting from depletion of endogenous EZH2 [35]. This evidence concerns the gene SCYL1 and neoplasm.