Epithelial-to-mesenchymal transition (EMT) has a crucial role in the transformation of cancer cells and the progression to an invasive phenotype. EMT is triggered by a number of signalling pathways – including Wnt/β-catenin signalling – leading to the expression of EMT-specific transcription factors and the subsequent downregulation of E-cadherin. β-catenin also functions in cell adhesion, where it links cadherins to α-catenin and the cytoskeleton. However, the molecular mechanism underlying the switch between its transcriptional and adhesion functions remains largely unclear. To address this question, Bo-An Li and co-workers (p. 5692) explore the role of Wnt/β-catenin signalling in hepatocellular carcinoma (HCC), which shows a particularly poor patient prognosis. The authors focus their attention on hepatocyte nuclear factor 4α (HNF4α) because it is a master gene of the hepatic lineage and has been implicated in regulating EMT. They now describe a double-negative feedback mechanism that controls Wnt/β-catenin signalling and HNF4α expression in vitro and in vivo; Wnt/β-catenin signalling during EMT reduces HNF4α activity, whereas HNF4α competes with β-catenin and inhibits the expression of EMT-related Wnt/β-catenin targets. Moreover, the authors suggest that HNF4α also regulates the switch between transcriptional and adhesion functions of β-catenin. These insights into the regulation of EMT might be exploited in approaches to block the invasive potential of HCC.