In agreement, we confirm the potent tumour-suppressive effects of TGFβ signalling in Apc-mutant cells22,40, which could help explain why multiple mutations (Wnt- and MAPK-activating) are required to tolerate epithelial TGFβ signalling and switch the cellular response to TGFβ from apoptosis to proliferation. The gene discussed is APC; the disease is neoplasm.