However, in comparison to previously described Fgfr1 and Fgfr2 mouse models of craniosynostosis, this one falls short of recapitulating the human disease; it has a very low craniofacial phenotypic penetrance with a sex bias opposite to what is seen in humans (Cornille et al., 2019). This evidence concerns the gene FGFR2 and craniosynostosis.