Indeed, it is hypothesised that the selective loss of TGFβ-mediated cytostatic responsiveness in the tumour epithelium allows for increased ligand production and secretion from the TME, which in turn promotes extracellular matrix remodelling, activation of cancer-associated fibroblasts (CAFs), epithelial-mesenchymal transition (EMT), angiogenesis, immune evasion, metastatic competence and drug resistance15–17. The gene discussed is TGFB1; the disease is neoplasm.