Using a low-molecular-weight compound that competes with p53 for binding into a hydrophobic cleft on the surface of MDM2, termed nutlin-3 [96], we have been able to elicit a robust and selective activation of the p53 pathway in NB cells with wild-type p53, leading to G1 cell cycle arrest, apoptosis, premature senescence and neuronal differentiation [97]. The gene discussed is TP53; the disease is neuroblastoma.