These findings provide novel insight into the β-catenin/TCF-dependent mechanisms of CRC carcinogenesis, suggesting that the relative amounts of β-catenin and those of different TCFs may ultimately dictate or relieve a default repression of nherf1 gene, in keeping with the notion that TCFs function as powerful transcriptional activators or repressors [40]. This evidence concerns the gene HNF4A and colorectal carcinoma.