French researchers have developed a recombinant protein therapeutic approach, based on a soluble form of human fibroblast growth factor receptor 3 (sFGFR-3), to treat mice with abnormal bone development caused by achondroplasia. This genetic disorder, which is characterized by short stature, is caused by a single point mutation in the gene FGFR3, which leads to prolonged receptor activation upon FGF binding. sFGFR-3 prevents ligand binding to the mutant receptor, thereby preventing excessive intracellular signalling and rescuing the symptoms of achondroplasia.