We sought in this investigation to ascertain whether Arf had p53-independent functions in suppressing tumor progression in the RIP-Tag2 PNET model, via crosses to mice carrying a genetic knock-out of Arf. A previous study showed that genetic knockout of p53 in this model did not result in an accelerated pathway to tumor formation, and in fact, beta tumor cell proliferation was reduced, likely a consequence of destabilization of the SV-40 large T antigen oncogene, to which it binds [17]. The gene discussed is TP53; the disease is neoplasm.