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In mammalian cells, BCL9 proteins contribute to, but may not be obligatory for, β-catenin–mediated transcription. BCL9L mRNA knockdown in a human colon cancer cell line induced an epithelial phenotype that was associated with the translocation of β-catenin from the nucleus to the cell membrane, suggesting that BCL9L might regulate the switch between the adhesive and transcriptional functions of β-catenin. BCL9L upregulation has been associated with breast and colon cancers, and BCL9 has recently been reported to enhance β-catenin–mediated transcription and increase the proliferation as well as the metastatic potential of tumor cells.