In contrast to WT ZM and its H4K20me1/2-binding-defective or ZnF-deleted mutants, the Tip60-interaction-defective mutants (ΔMBTx4 or ALL > DDD) failed to arrest terminal differentiation (Fig. 5e) and failed to maintain high expression of ZM’s pro-oncogenic targets such as Hoxa9, Meis1, Sox4, Myc and Myb (Fig. 5f). Here, HOXA9 is linked to acute lymphoblastic leukemia.