This suggests that nearly half the differences in brain-skull integration between Fgfr2+/S252W Apert syndrome mice and Fgfr2cC342Y/+ Crouzon syndrome mice are due to the developmental architecture and variation in the “background” genomes of these particular samples, while the remaining differences are due to the interaction of each craniosynostosis-associated mutation with the respective genomes of those strains. Here, FGFR2 is linked to craniosynostosis.