This observation is supported by other authors, who similarly encountered a cytosolic accumulation of β-catenin in adenomas as well as in adenocarcinomas using the same experimental model.[73, 75] In human colon cancer, the cytosolic accumulation of β-catenin is either caused by mutational inactivation of the AP C tumor suppressor gene or by mutation of β-catenin itself leading to nuclear translocation and binding to TCF4 (T-cell Factor 4). This evidence concerns the gene APC and adenocarcinoma.