The enhanced proliferation and evasion of apoptosis in NB caused by this variant were through BARD1β interaction with and stabilization of Aurora kinases A and B. The mechanisms of BARD1β were independent of p53 and BRCA1-dependent HR because silencing of BARD1β did not alter the level of phosphorylated p53 and additional silencing of PARP1 was not lethal to NB cells. This evidence concerns the gene TP53 and neuroblastoma.