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. The gene discussed is AURKA; the disease is neuroblastoma.