The series of different Apc and Ctnnb1 mouse models that we employed have previously been used to show that β-catenin activity levels are selected for by different types of cancer, and these ectopic increases in signalling activity can also lead to a range of developmental defects (Kielman et al., 2002; Gaspar et al., 2009; Buchert et al., 2010; Bakker et al., 2013). The gene discussed is APC; the disease is cancer.