A second approach has taken advantage of the fact that deletions or inactivating mutations in the genes and proteins of the β-catenin destruction complex, such as Apc (adenomatous polyposis coli) (Fig. 2), also lead to the over-activation of the WNT/β-catenin pathway and tumour formation (e.g. in intestinal cancers in mouse and humans) [87, 88]. The gene discussed is APC; the disease is neoplasm.