This confirms that, in principle, cellular SAMHD1 and DCK levels are involved in determining AML cell sensitivity to CNDAC (and cytarabine), although, as shown in this study, intrinsic and acquired CNDAC resistance differ in AML cells in that intrinsic CNDAC resistance is predominantly driven by high SAMHD1 levels and acquired CNDAC resistance by a reduction in DCK. This evidence concerns the gene DCK and acute myeloid leukemia.