In a study of a mouse model of ACH (Fgfr3Y367C/+), our research group previously reported on abnormal mandibular shapes, mandibular hypoplasia, and defective chondrocyte proliferation and differentiation affecting MC and condylar cartilage.10,24 The impact of activating Fgfr2 mutations in craniosynostoses has also been investigated in mouse models of Apert, Crouzon and Pfeiffer syndromes, with the observation of abnormal microarchitectures and mineralization of the developing mandible.25 The gene discussed is FGFR2; the disease is Pfeiffer syndrome.