The enhanced cancer specific activity of the ERE73 (1 + 2)-ARF (−13) and ERE73 (3 + 4)-ARF (−13) constructs is mediated by deregulated E2F activity, since it was abolished by mutation of E2F binding sites of ERE73s (Figure 2D), and introduction of a constitutively active form of pRB in cancer cell lines, to suppress E2F, diminished the activities of ERE73s-ARF (−13) promoters (Figure 2E). This evidence concerns the gene CDKN2A and cancer.