We also reported that although Shox2Shox–KI/KI mice did not exhibit TMJ dysplasia and ankylosis at birth, a phenotype observed in mice carrying inactivation of Shox2 in the cranial neural crest lineage, the mice did develop a different TMJ defect, a premature wearing out of the articular disc postnatally [2,13,14]. The gene discussed is SHOX2; the disease is ankylosis.