The focal adhesion protein Kindlin2 is well known to regulate inside-out integrin signalling and, hence, cell-matrix adhesion. However, its roles during development remain poorly understood, at least partly because complete depletion leads to early lethality in both mouse and frogs. Hui Zhao and colleagues set out to investigate the function of Kindlin2 knockdown in Xenopus, and find that it is required for neural crest. Through morpholino and CRISPR-mediated loss-of-function approaches in X. laevis and X. tropicalis, they show that kindlin2 depletion leads to impaired expression of early neural crest markers. Loss of kindlin2 disrupts FGF signalling, which is known to be important for neural crest specification, apparently by decreasing the stability of the FGF receptor. This function of Kindlin2 is integrin-independent, as mutants unable to bind integrins can still rescue the kindlin2 knockdown phenotype. Although the mechanism by which Kindlin2 stabilises FGF receptors has yet to be determined, this work adds to an emerging picture of integrin-independent roles for Kindlin2 in signalling pathway regulation. Furthermore, this work identifies a key player in early neural crest specification in the vertebrate embryo.