The disease is difficult to study because available cell lines and animal models are poorly representative of the underlying biology—cell lines lack the phenotypic diversity seen in the oesophageal submucosal glands, and mouse models do not accurately model neoplastic progression.55,56 Through the use of CRISPR/Cas9 technology, patient biopsy-derived Barrett’s organoids that lack APC have been generated and used to demonstrate a fundamental role of aberrant Wnt/β-catenin signalling in the neoplastic progression of Barrett’s-associated oesophagus.57 This evidence concerns the gene APC and digestive system neoplasm.