Although the mechanisms underlying chemoresistance in AML have not been fully elucidated, substantial evidence indicates that decreased deoxycytidine kinase (dCK) activity and reduced expression of the human equilibrative nucleoside transporter 1 (hENT1) are major determinants of cytarabine resistance in AML patients and leukemia-derived sublines [10,11,12,13]. Here, DCK is linked to acute myeloid leukemia.