These include ribonucleotide diphosphate reductase (RNR) inhibitors, which increase Ara-CTP levels in AML blasts2; however, these nucleoside analogs also rely on phosphorylation by dCK, rendering them ineffective towards Cytarabine-resistant clones lacking dCK activity19,23,24. The gene discussed is DCK; the disease is acute myeloid leukemia.