To examine the feasibility of using deregulated E2F activity and tumor suppressor gene promoters to drive gene expression specifically in cancer cells, we constructed artificial promoters, in which E2F response elements of the TAp73 promoter (ERE73s) are tandemly conjugated to the ARF core promoter, and compared their cancer cell specificity with those of promoters harboring E2F binding site mutations in ERE73s. The gene discussed is CDKN2A; the disease is neoplasm.