For example, mutations in mice MSX1 result in craniofacial abnormalities that include cleft palate and absence of specific teeth [19], [20], while mice expressing a mutated MSX2 transgene exhibit the symptoms of craniosynostosis, a disease characterized by premature closure of the cranial sutures [16], [21], more severely, double mutants of MSX1and MSX2 exhibit a severe limb phenotype [22]. Here, MSX2 is linked to craniosynostosis.