Analysis of 3D reconstructions of chondrocrania of the Fgfrc^C342Y/+ Crouzon syndrome mouse show the direct effects of this Fgfr2 mutation on embryonic cranial cartilage formation and the indirect effects of chondrocranial morphology on cranial dermal bone development.

Homology of vertebrate skull structures should be based on evolutionary continuity and an appreciation of germ layer origins and inductive signaling in the embryonic head.

Quantitative analyses associating the morphology of developing organs with dynamic gene expression patterns can reveal biological phenomena that cause malformations and malfunction but remain elusive to traditional qualitative assessments.

Ts65dn mice exhibit structural, functional, molecular, and genetic alterations that are modulated but unrecovered by prenatal chronic GTE-EGCG, highlighting the importance of holistic studies to understand complex disorders and treatments.

A four-switch long-range allosteric network controls FGF receptor kinase conformational dynamics as well as activity and is applicable to other receptor tyrosine kinases.