In addition, even after multiple rounds of dose-intensive chemotherapy, a large majority of recurrent neuroblastomas maintain p53 functionality.26,27 This suggests that for neuroblastoma patients with both de novo and relapsed situations, reactivation of p53 and induction of p53-dependent apoptosis may be an effective therapeutic strategy.26,27 The oncogene MDM2 is the major negative regulator of p53 and has become the focus of such molecular targeting.7,8 MDM2 dramatically shortens the protein half-life of p53 by initiating ubiquitination via its E3 ligase activity. The gene discussed is MDM2; the disease is neuroblastoma.