We further discovered that compared to that in normal bone marrow cells, RUNX3 in AML cells tended to bind genes enriched in DNA repair (Chek1, Ddb1, Rad51c, and Rpa2), antiapoptosis (Bcl2, Bcl2l10, Bcl2l12, and Mcl1), and leukemogenesis (Myc, Cd93, Kit, Ikzf2, Fto, and Sox4) pathways. This evidence concerns the gene BCL2 and acute myeloid leukemia.