They also demonstrated that AML cells devoid of KDM6A were more resistant to treatment with the chemotherapeutic agents cytarabine and daunorubicin, a consequence of reduced expression of the drug influx transporter ENT1, and that re-expression of KDM6A supressed proliferation and restored responses to cytarabine (Fig. 2) [25]. Here, KDM6A is linked to acute myeloid leukemia.