Wnt/β-catenin signalling regulates cell proliferation and fate determination throughout development. Stabilisation of β-catenin is essential for Wnt signalling activation, and although clathrin, through its role in endocytosis, has been associated with this stabilisation, its specific function is still debated. In this study, Eva Wenzel and colleagues (Munthe et al., 2020) now determine that clathrin is involved in Wnt/β-catenin signalling by regulating intracellular trafficking of newly synthesised Wnt pathway components. Depletion of clathrin in cell culture leads to a reduction in β-catenin protein levels, both of the membrane-bound and the soluble cytosolic pools. This decrease is independent of endocytosis, as the depletion of the clathrin adaptor protein AP-2 does not result in the reduction of β-catenin levels; similarly, inhibiting the clathrin-dependent formation of intraluminal vesicles does not affect β-catenin levels. Instead, clathrin-depleted cells show defects in the anterograde trafficking of transmembrane proteins that are important for β-catenin stabilisation, such as the Wnt co-receptor low-density lipoprotein receptor-related protein 6 (LRP6) and cadherin molecules. Thus, this study sheds light on the impact of clathrin in Wnt/β-catenin signalling, shifting the focus away from endocytosis and highlighting its role in regulating anterograde transport and activation of Wnt signalling.