Moreover, recent mouse model studies have demonstrated that long bone length can be restored in achondroplasia by targeting the mitogen-activated protein kinase (MAPK) pathway, which is activated by the tyrosine kinase receptor FGFR3 mutations in achondroplasia, and causes a disruption to normal chondrocyte differentiation (33). This evidence concerns the gene FGFR3 and achondroplasia.