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Missense mutations in Fibroblast Growth Factor Receptor 3 (FGFR3) result in several human skeletal dysplasias including the most common form of dwarfism achondroplasia. The NIH announces the generation of FGFR3 knockin mice which have a Gly369Cys mutation inserted into the mouse genome. Phenotypic analysis of the mice reveals that the FGF/FGFR3 signals affect both chondrogenesis and osteogenesis by regulating Stat proteins and cell-cycle inhibitors and the activities of chondrocytes osteoclasts and osteoblasts during endochondral ossification. These mice provide a new animal model to study functions of FGF/FGFR3 signals in achondroplasia patients which could lead to new drug discovery and therapeutic treatments. We will provide 60 embryos.