We next tested directly whether tumor growth was dependent on both p53 and MYCN by generating GTML mice deficient in functional p53, using a mouse model in which the endogenous Trp53 gene is replaced with a knockin allele (Trp53KI) encoding a 4-hydroxytamoxifen (4-OHT)-regulatable p53ERTAM fusion protein (Christophorou et al., 2005). Here, MYCN is linked to neoplasm.