Our previous analyses showed that despite coronal craniosynostosis in mice carrying Fgfr2 Apert syndrome mutations, at P0 the facial skeleton is the most affected region of the skull with phenotypic differences between Fgfr2+/S252W and Fgfr2+/P253R mutant mice restricted to the posterior aspect of the palate [9]. The gene discussed is FGFR2; the disease is Apert syndrome.