Here, we show that treatment of AML cells with a novel ETP, NT1721, depleted DNMT1, EZH2 and BMI1 and concomitantly increased the expression of the tumor suppressor genes CDKN2A (p16), CDKN2B (p15) and BIM: Up-regulation of BIM may enhance apoptosis induction since a previous study showed that silencing of BIM promotes apoptosis resistance in leukemia [51]. The gene discussed is CDKN2B; the disease is acute myeloid leukemia.