FGF signalling is implicated in salivary gland branching during development, but the mechanisms underpinning its role in this process are unknown. Here, Ayan Ray and Philippe Soriano focus on the FGFR1 and FGFR2 receptors, which they show are particularly strongly expressed in outer bud epithelial cells of murine salivary glands. They generate various compound mutants to disrupt Fgfr1 and/or Fgfr2 expression in the salivary gland epithelium and find that this results in branching defects. They are able to largely rescue these defects by reintroducing Fgfr1/2FCPG alleles encoding receptors that cannot engage their standard downstream signals, which suggests that these receptors are regulating salivary gland branching through non-canonical mechanisms. They go on to demonstrate that loss of FGF signalling results in reduced E-cadherin accumulation at cell-cell junctions, reduced cell adhesion to the basement membrane, and compromised basement membrane integrity. Again, they partially rescue these cell-cell and cell-matrix adhesion defects by expression of the Fgfr1/2FCPG mutant alleles. Although the mechanisms underlying these effects remain to be determined, this work suggests non-canonical FGF signalling promotes proper salivary gland branching during development by modulating cell adhesion.