Evidence gathered from both models suggests these clusters act in a paracrine manner, driving tumour growth and/or invasion into surrounding tissues through the secretion of a wide range of factors (e.g. SHH, FGFs, BMPs, TGFB1; as well as pro-inflammatory mediators such IL1, IL6 and other CXC and CC chemokines) [1, 2, 14, 17, 41, 53]. The gene discussed is TGFB1; the disease is neoplasm.