The more profound effects observed upon loss of B9/B9L binding to β-catenin, compared to a loss of binding to Pygopus, are consistent with a recent report demonstrating that B9/B9L sustains β-catenin transcriptional activity in colorectal cancer cells and in developing forelimbs in a Pygopus-independent manner [18]. The gene discussed is BCL9L; the disease is colorectal cancer.