Although signalling through the Wnt/β-catenin pathway is associated with pancreatic ductal adenocarcinoma, only now has this pathway been shown to be critical for tumorigenesis. This was shown through experiments on β-catenin-null acinar cells, which could not undergo metaplastic transformation to ductal cells—a process central to the development of premalignant lesions. Furthermore, targeting the Wnt pathway with a specific antibody (OMP-18R5) in a transgenic mouse model of pancreatic cancer revealed normal acinar structures and fewer lesions than untreated mice.