Specifically, disrupting PRC2 allosteric activation can override the hyperactivity of EZH2Y641X and inhibit the proliferation of PRC2/EZH2-addicted tumors, providing a potential therapeutic strategy for PRC2/EZH2-addicted cancers by targeting EZH2SRM–EZH2SET-I and EZH2SRM–EED interactions (Lee et al., 2018a). Here, EZH2 is linked to cancer.