KMT2C/MLL3 and KMT2D/MLL2 methyltransferases along with the histone demethylase KDM6A/UTX are members of the activating MLL2-KDM6A/UTX complex [79], their deregulation due to cooperating mutations or aberrant splicing events, could provide an alternative mechanism to recurrent alterations of PRC2 members EZH2, SUZ12 or EED in T-ALL. This evidence concerns the gene EED and acute lymphoblastic leukemia.