A large-scale genomics screen of ampullary adenocarcinoma patients revealed frequent loss-of-function mutations of ELF3, consistent with its role as a tumour suppressor.14,15 In conjunction with these ELF3 inactivating mutations, altered levels of Wnt signalling were observed and it was found that silencing of ELF3 promoted motility and invasion of normal human epithelial cells. Here, ELF3 is linked to ampulla of vater adenocarcinoma.