FGFR2 and craniosynostosis: We previously generated a mouse model for Apert syndrome (AS) bearing FGFR2‐Ser250Trp (S250W) corresponding to human FGFR2‐S252W.[14] This mutation occurs in the extracellular domain, enhances ligand‐binding capability, and alters ligand specificity.[15, 16] The mutant mice presented with severe craniosynostosis characterized by premature coronal suture fusion and shortened cranial bases.