More recently, Schneider C and colleagues found that ara-CTP is hydrolyzed by the deoxynucleoside triphosphate (dNTP) triphosphohydrolase SAM domain and HD domain 1 (SAMHD1), which promotes the detoxification of intracellular ara-CTP pools [12]. Disruption of SAMHD1 increases Ara-C sensitivity in both cultured leukemia cells and mouse model of AML [13]. Here, SAMHD1 is linked to acute myeloid leukemia.