Muenke syndrome in humans, characterized by craniosynostosis with uni- or bicoronal synostosis, comes from an FGFR3 Pro250Arg mutation resulting in the increased binding affinity of FGFR3 to its ligand (Muenke et al., 1997; Ibrahimi et al., 2004), such as FGF9, by the substitution of a bulkier residue. Here, FGF9 is linked to craniosynostosis.