As p53-mediated tumor suppression is linked to upregulation of ARF (the alternative product of the Cdkn2a gene locus) by hyperactivated oncogenes like Ras [50,51,52], and mice lacking ARF primarily develop undifferentiated sarcomas [53], it was not surprising when Kirsch et al. demonstrated that conditional KrasG12D/+;Cdkn2aflox/flox mice efficiently develop UPS [54]. The gene discussed is TP53; the disease is neoplasm.