To functionally assess whether interaction with the NuA4/Tip60 complex is required for ZM-induced transformation, we introduced into ZM the damaging mutations that we have shown by coIP to abolish ZM:Tip60 interaction (Fig. 5a, b), which include a deletion of MBT repeats (ΔMBTx4) and ALL > DDD, triple point mutations (A661D/L684D/L688D) of MBTD1’s MBT1-2 motifs recently shown to disrupt hydrophobic binding of WT MBTD1 to EPC1, a subunit of NuA4/Tip60 complex22. The gene discussed is KAT5; the disease is acute lymphoblastic leukemia.