In light of the potent effect of p53 loss on both CD2‐RUNX2 and CD2‐MYC lymphoma development, it was surprising that the combination of both transgenes led to the rapid development of tumors in which the p53 pathway appears to be intact.18 In support of this interpretation, the wild‐type p53 allele is retained in primary tumors in CD2‐RUNX2/CD2‐MYC/p53+/− mice, but rapidly lost on in vitro culture of lymphoma cell lines which also display de novo activation of the p53‐repressed target p19Arf. The gene discussed is RUNX2; the disease is lymphoma.