SLC25A51 and acute myeloid leukemia: Taken together, we hypothesize that the oncogenic potential of SLC25A51 in AML may be attributed to its capacity to transfer NAD+ into mitochondria, thereby enhancing the activity of the NAD-dependent enzymes SIRT3, SIRT4, and SIRT5 located in mitochondria, which ultimately promotes the malignant proliferation of AML cells (50).