Generally, the genetic cause of classical cleidocranial dysplasia in humans is heterozygous loss of RUNX2, not MSX2. However, the hyoid phenotypes of Runx2+/− and Tbx1−/− are different, indicating that Tbx1 might have a primary role in early patterning and perichondral ossification in the hyoid bone [175]. Here, TBX1 is linked to cleidocranial dysplasia 1.