Disturbed the Sp1/NF-κB complex on DNMT1, DNMT3a, and DNMT3b promoter thereby decreasing the transactivation activity of these complexes and downregulating their mRNA and protein expression levels in AML cells in vitro and in vivoInduced a cell cycle arrest in the S-phaseIncreased SubG1 cell fraction. The gene discussed is DNMT3A; the disease is acute myeloid leukemia.