Insights into the functional significance of the β-catenin accumulating cells have suggested that these clusters act as signal “hubs,” secreting a plethora of growth factors and cytokines (e.g., SSH, FGFs, BMPs, TGF-β1, IL1, IL6) (16–18), which activate specific pathways in nearby non-accumulating tumor cells, driving tumor infiltration into surrounding tissues in an autocrine/paracrine manner (19, 20). The gene discussed is CLN5; the disease is neoplasm.