In the light of the well-documented role of BCL9 in facilitating β-catenin-dependent transcription, it was puzzling that the conditional double-knockout of Bcl9 and B9l in the intestinal epithelium (Bcl9/B9l DKO below) did not reduce the tumour numbers in mouse models based on colitis and chemically-induced β-catenin-dependent tumours18, or on weak attenuation of Apc function19. Here, BCL9L is linked to neoplasm.