Considering that EZH2 overexpression has been observed at progressively increasing levels from low-risk, to high-risk MDS, to AML [19] it makes sense that loss-of-function UTX mutations (equivalent to EZH2 overexpression) are late events in leukemogenesis and that the mutual exclusion of loss-of-function EZH2 and UTX mutations is likely the result of repression of leukemic growth through opposing effects. The gene discussed is EZH2; the disease is acute myeloid leukemia.