Gain-of-function mutations in fibroblast growth factor receptor 1 (FGFR1), FGFR2 and FGFR3 are responsible for many craniosynostosis syndromes, including bent bone dysplasia and Crouzon, Apert, Pfieffer, Beare–Stevenson and Muenke syndromes, among others. This evidence concerns the gene FGFR1 and bent bone dysplasia.