Interestingly, mutations in the same FGFR (either FGFR1, FGFR2 or FGFR3) can result in different craniosynostosis syndromes, thus implicating a common pathologic mechanism with FGFR gain of function in Pfeiffer, Apert, Muenke, and Beare-Stevenson syndromes [5]. This evidence concerns the gene FGFR2 and Beare-Stevenson cutis gyrata syndrome.