LOF mutants of EZH2 (G266E, T393M, and C606Y) that result in loss of PRC2 function and drive Notch signaling activation, and increase the in vivo tumorigenic potential of T-ALL cells, suggesting that PRC2 may have a tumor-suppressor function, although the specific mechanisms remain to be further explored (Figure 5A) [192]. Here, EZH2 is linked to neoplasm.