Therefore, the analysis results that there was a constant expression levels of TFRC in AML cells encouraged us to generate the Ara-C@HFn in this study, which had the potential to reduce the adverse effects of free Ara-C on AML therapy and had a more potent antineoplastic effect in AML than free Ara-C, which was as expected. The gene discussed is TFRC; the disease is acute myeloid leukemia.