In acute myeloid leukemia patients, higher expression of NT5C2 related to poor prognostic.[7–9] In lung tumor cells, the silence of NT5C2 opposes the cancer phenotype, activates the p53/AMPK pathway and regulates metabolism.[10,11] Raza et al[12] showed that NT5C2 deficiency facilitates tumor growth, response to chemotherapeutic and migration. Here, NT5C2 is linked to acute myeloid leukemia.