It is caused by a single point mutation in the gene coding for FGFR3, which leads to prolonged activation upon ligand binding.58 These independent observations can be interpreted as indicating that FGF2 might be overexpressed in OVX rats, leading to impaired epiphyseal growth plate, and the blockade of FGF2 action by APT-F2P ameliorates the epiphyseal growth plate and might cure achondroplasia. The gene discussed is FGFR3; the disease is achondroplasia.