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AML cells are much more sensitive to PARP inhibitors when NAD+ depletion is present because it not only prevents PARP-mediated repair of DNA single-strand breaks but also causes homologous recombination defective (HRD) phenotypes by down-regulating SIRT6s deacetylation activity, which results in hyperacetylation and transcriptional repression of the BRCA1 promoter region (121)

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The visceral fat deposition was also found to be reduced, along with decreased plaque macrophages and smaller aortic plaques [56]