Not only did expression of claudin-1 decreased significantly in response to the reduction of intracellular β-catenin by adenovirus mediated transfer of wild-type APC into the APC-deficient colon cancer cells, but also two putative Tcf4 binding elements in the 5' flanking region of claudin-1 were confirmed to be responsible for activating its transcription [69]. The gene discussed is APC; the disease is colonic neoplasm.