BCL9 and neoplasm: This, together with the scaffolding role of Bcl9, readily explains why the transcriptional profile of the QKO tumours is largely determined by Bcl9 loss (Fig. 3b, c) and, by implication, why the latter has such a profound impact on β-catenin-dependent intestinal neoplasia in both Apc models (Figs 1a and 6b).