During development, enteric neural crest-derived cells (ENCCs) migrate and colonise the length of the gut to form the enteric nervous system (ENS). In Hirschsprung disease, however, ENCCs arrest in the colon, resulting in the absence of an ENS in the hindgut. Now, Nandor Nagy and colleagues investigate the role of the caecum (found at the junction between the small and large intestine) in regulating ENCC migration into the colon. Using immunofluorescence staining of cultured chick guts, the authors show that removing the caecal buds stops the proliferation of ENCCs at the hindgut junction, where they terminally differentiate into neurons. In addition, through transplantation experiments, the authors show that ENCCs that travel into the hindgut are exclusively cells from the caecal buds. RNA sequencing of this new niche reveals that components of the non-canonical Wnt signalling pathway (such as Wnt11) are upregulated in caeca. Indeed, providing Wnt11 to cells in culture prevents neuronal differentiation and permits ENCC migration. Together, these results reveal the indispensable role of the caeca in development of the hindgut ENS by providing a niche to maintain ENCC stemness through non-canonical Wnt signalling.