A new study in mice suggests that blockade of β-catenin signalling has promise as a new therapeutic strategy against MEN1-deficient pancreatic neuroendocrine tumours (NETs). Lack of menin, the protein encoded by MEN1, activates β-catenin signalling in mouse and human pancreatic NETs. Genetic or pharmacological suppression of β-catenin signalling inhibited tumour growth, decreased hyperinsulinaemia and hypoglycaemia, and improved survival in mice with MEN1-deficient pancreatic NETs.