We hypothesized that UBE4B would interact with members of DNA damage and repair and apoptotic pathways, potentially mediating the observed associations between UBE4B expression and patient outcomes, and we therefore hypothesized that regulation of the levels of the Ku70 and c-FLIPL proteins by UBE4B-mediated ubiquitination would impact responses of neuroblastoma tumors to therapy and contribute to the observed associations between UBE4B expression and patient outcomes. The gene discussed is CFLAR; the disease is neuroblastoma.