The FGFR3G380R activating point mutation, associated with the most common form of human dwarfism, achondroplasia, leads to the shortening of both long and craniofacial bones due to premature growth plate hypertrophy and synchondrosis fusion.33,34 Similarly, constitutive activation of the downstream FGFR3 effector, MEK1, in chondrocytes35,36 causes premature synchondrosis fusion, mirroring the phenotype observed in Fgfr3G374R mice, which models the orthologous human mutation. Here, FGFR3 is linked to achondroplasia.