Studies of morphological integration (MI) reveal an elevated magnitude of association between chondrocranium and dermatocranium of Fgfr2cC342Y/+ mice at E15.5 matching the results of previous analyses of the skulls of Fgfr2+/S252W and Fgfr2+/P253R Apert syndrome mouse models at P0 (Martínez-Abadías et al., 2011) that suggested FGF/FGFR signaling as a covariance-generating process in skull development acting to modulate MI intensity. The gene discussed is FGFR2; the disease is Apert syndrome.