Interestingly, most FGFR3 was localized within the nucleus, similar to the FGFR3 distribution associated with Fgfr3 activating mutations causing achondroplasia.72 Moreover, nuclear translocation of FGFR3 protein has also been tied to aberrant proliferation in breast and prostate cancers.73,74 Thus, RUNX2 deficiency in synchondrosis chondrocytes leads to elevated FGFR3 and possible receptor nuclear translocation, which may explain subsequent aberrant endochondral ossification and premature synchondrosis fusion. This evidence concerns the gene FGFR3 and achondroplasia.