DCTD (dCMP deaminase) catalyzes the deamination of dCMP to dUMP, providing a critical substrate for thymidylate synthase in nucleotide biosynthesis. The enzyme also participates in a salvage pathway that eliminates epigenetically modified cytosine derivatives, converting 5-hydroxymethyl-dCMP to 5-hydroxymethyl-dUMP, which is subsequently hydrolyzed to 5-hydroxymethyluracil and deoxyribosephosphate. DCTD has emerged as a determinant of chemotherapy sensitivity in hematologic malignancies. Loss of DCTD confers resistance to decitabine (5-aza-dC), a nucleoside analogue used to treat myelodysplastic syndrome and acute myeloid leukemia, suggesting that DCTD-mediated conversion of decitabine metabolites is required for cytotoxicity 1. In malignant glioma, elevated DCTD expression correlates with shortened overall survival, positioning the enzyme as a prognostic marker 2. Recent evidence indicates that DCTD may suppress ferroptosis in glioblastoma, identifying it as a potential therapeutic target in this context 3. These findings suggest DCTD inhibition could enhance decitabine efficacy in resistant hematologic cancers, while DCTD suppression may sensitize glioblastoma to ferroptosis-based therapies. The gene's roles in nucleotide metabolism and drug activation underscore its relevance to cancer treatment outcomes.