Given that the timing of Eμ-myc-driven tumor development can be influenced by strain background [26] and breeding strategy, we can only surmise that these potential differences or the specific E2f1-null allele [27],[28] used in our studies versus that of Baudino and colleagues are sufficient to account for the discrepant effects of E2F1 deficiency. Here, E2F1 is linked to neoplasm.