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Several reports have shown that by inhibiting mitochondrial processes such as the oxidation of fatty acids, the activity of the electron transport chain (ETC), the replication of mtDNA, or the synthesis of mitochondrial proteins, the sensitivity to Ara-C increases in vitro and in vivo (Farge et al., 2017), and the proliferation of primary AML cells have slightly decreased (Vitkeviien et al., 2019)

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