Finally, while numerous properties of E2F1 and E2F2, including gene repression and the promotion of apoptosis and DNA repair, have been suggested to underlie observed increases in tumors in E2f1 and E2f2 mutant mice (reviewed in [11,12]), we demonstrate that the promotion of Bcr-Abl-dependent leukemias and the expansion of p53 mutant cells by E2f1/E2f2 disruption result from non-cell autonomous consequences of E2f loss. This evidence concerns the gene TP53 and leukemia.