EZH2 gain-of-function mutations that enhance H3K27me3 levels are pathogenic for germinal center type large B cell lymphomas [5], [6], whereas global loss of EZH2 function due to mutation/deletion of EZH2 or associated factors such as SUZ12, EED and ASXL1 are associated with myeloid neoplasms [7]–[9]. Here, EZH2 is linked to myeloid neoplasm.