While in patients with familial adenomatous polyposis (FAP) β-catenin is not degraded through inactivating mutations in APC, most sporadic DTF harbor alterations in CTNNB1; both leading to a nuclear accumulation of β-catenin and an oncogenic activation of the Wnt/β-catenin signal transduction pathway3–6. The gene discussed is APC; the disease is Familial adenomatous polyposis.