These data demonstrate the close link between expression of a stress-responsive genetic program and resistance to daunorubicin through upregulation of ABCB1; they further demonstrate that chemotherapy treatment with daunorubicin activates a stress-responsive enhancer and induces upregulation of a drug resistance mechanism in AML blast cells that may contribute to therapeutic failure and disease relapse. This evidence concerns the gene ABCB1 and acute myeloid leukemia.