Although the determinants underlying the different fates of BRAF-mutant cells in these two models remain unclear, the implications are profound: While reversion of Lgr5+ ISCs to a foetal-like state, in the absence of TGFβ signalling, fuels aggressive BA tumour growth, conversion to a TA-like state leads to exhaustion of the cancer stem cell pool and clonal extinction. The gene discussed is TGFB1; the disease is neoplasm.