EED and neoplasm: EZH1, a paralog of EZH2, can also form functional PRC2 complexes as a compensatory mechanism for tumor cells to escape EZH2 inhibition.490,491 Therefore, co-inhibition of EZH2 and EZH1492–494 or EED inhibition492,495 could more completely inhibit the activity of PRC2, especially in the presence of innate or acquired resistance mutations in EZH2 and by addressing the potential compensatory mechanism of EZH1-driven tumor growth.