Mouse models of ACH with Fgfr3 activation mutations (Fgfr3G369C/+, Fgfr3G380R/G380R, and Fgfr3Y367C/+) also exhibited defective bone formation, a decrease in femoral bone mass, and changes in bone microarchitecture in growing and adult mice (20, 27, 28). This evidence concerns the gene FGFR3 and achondroplasia.