Although the mechanisms underlying chemoresistance in AML are not yet fully understood, accumulating evidence indicates that reduced activity or loss of function of the equilibrative nucleoside transporter 1 (ENT1) and deoxycytidine kinase (dCK) contributes significantly to Ara-C resistance in both AML patients and leukemia cell models [3,4,5,6,7]. This evidence concerns the gene DCK and leukemia.