Together, these results suggest that disruption of the DNA damage checkpoint through inactivation of CHK1 and CHK2, rather than their upstream kinases ATM and ATR, as well as interfere with the DNA repair machinery by downregulating DNA repair proteins (e.g., Rad51), might account for or at least contribute to the synergistic interaction between chidamide and MI-3 in AML cells carrying MLL-rearrangement. The gene discussed is CHEK1; the disease is acute myeloid leukemia.