Disruption of these E-cadherin homotypic interactions results in the release of β -catenin from E-cadherin and subsequent translocation of β -catenin into the nucleus; the nuclear β-catenin associates with TCF4 (a member of transcription factor family) to form a β-catenin/TCF complex and activates the transcription of genes involved in cancer initiation, progression and metastasis such as c-Myc, and uPAR [26]. This evidence concerns the gene CDH1 and cancer.