It has been suggested that AURKB is a direct target of transcription factor E2F (29). Furthermore, when we interrogated the ENCODE database, we found chromatin immunoprecipitation evidence for binding of E2F transcription factors to the proximal promoters of the AURKB, ESCO2, SUV39H1, and WHSC1 genes, whereas CIITA, KDM6B, and NCOA1 had no such sites. We, therefore, investigated whether the effects of IFN-γ or IL-4 on AURKB, ESCO2, SUV39H1, and WHSC1 could be reversed by adenovirus-mediated overexpression of E2F1. Infection with the E2F1 expressing virus increased E2F1 protein (Figure 7A) and, as expected, the mRNA levels of the known E2F responsive genes, Cyclin E and PCNA (38) (Figures 7B,C). E2F1 gene transfer completely reversed the inhibitory effect of IFN-γ and IL-4 on AURKB, ESCO2, SUV39H1, and WHSC1 mRNA levels (Figures 7D–G), except in the case of AURKB for which the effect of IL-4 was only partly reversed (Figure 7D). These data provided further support for the conclusion that the effects of IFN-γ or IL-4 on these genes were, at least partly, mediated indirectly through inhibition of proliferation.