Moreover, initial research on targeted treatment for MEF2D fusion BCP-ALL mainly focused on the high expression of HDAC9 using HDAC inhibitors.7,12,15 In the MH/NRASG12D leukemic model, the HDAC inhibitor Panobinostat, when combined with conventional chemotherapy, could effectively extend the survival of mice.12 These efforts, nevertheless, were constrained by relatively small scale of compound screenings and the limited diversity of screening model systems.16,17. This evidence concerns the gene HDAC9 and acute lymphoblastic leukemia.