The impact of Fgfr2-activating mutations on MC homeostasis has already been studied in Fgfr2 craniosynostosis mouse models of Apert, Crouzon and Pfeiffer syndromes.25,27 Low proliferation in MC (E15.5) and in the forming mandible (E17.5) has been observed in Fgfr2cC342Y/+ embryos.27 In contrast to the situation for the Fgfr3N534K/+Hch mouse model, we did not observe a significant impact of the Fgfr2cC342Y/+ mutation on chondrocyte differentiation in MC in our Crouzon embryos at E16.5 (data not shown). This evidence concerns the gene FGFR2 and craniosynostosis.