The same could also explain why the Bcl9-deleted ApcMin intestines exhibited hundreds of tiny adenomas (Fig. 1): evidently, their growth was stunted, owing to their dysfunctional β-catenin-dependent transcription (Fig. 2 and Supplementary Figure 6), but they appeared to be retained more efficiently within intestinal crypts owing to their high levels of cell surface β-catenin (Fig. 6b). This evidence concerns the gene BCL9 and adenoma.