Many groups have studied the roles of the PRC2 components, especially EZH2 and EED, with contradictory findings regarding PRC2 activity in mouse models of AML; some groups identified PRC2 as necessary for leukemogenicity, while others found that the loss of PRC2 components confer enhanced leukemic capacity.80-82 A seminal study by Basheer et al. elucidated these contradictory findings and attributed these to the disease stage.83 They discovered that EZH2 and PRC2 play an oncogenic role at disease onset and a tumor-suppressive role during disease maintenance. Here, EED is linked to acute myeloid leukemia.