Treatment of the N-Myc-amplified neuroblastoma cells with combination of IFN-γ and retinoic acid down regulates N-Myc expression through increased protein turnover, upregulates Mad1 mRNA and protein, and reduces N-Myc/Max heterodimerization, and predominates Mad1/Max network resulting in repression of the N-Myc target genes and potentiating differentiation and growth inhibition in neuroblastoma cells [39] (Figure 2). The gene discussed is MAX; the disease is neuroblastoma.