To determine whether the increased cancer cell specificity of ERE73 (1 + 2)-ARF (−13) and ERE73 (3 + 4)-ARF (−13) is due to deregulated E2F activity in the cancer cell lines, we introduced point mutations (MTs) in the ERE73 (1 + 2) and ERE73 (3 + 4) response elements, which successfully abrogated E2F responsiveness in our previous report (Figure 2A) [39]. The gene discussed is CDKN2A; the disease is cancer.