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 SIRT6’s deacetylation activity, which results in hyperacetylation and transcriptional repression of the BRCA1 promoter region (121). This evidence concerns the gene PARP1 and acute myeloid leukemia.