The heterozygote Prkar1a activating point mutation R368X knock-in mice (Prkar1a[R368X]/[+] mice) had chondrodysplasia and peripheral acrodysostosis affecting the endochondral skeleton, which resulted in shorter tails, shorter length and shorter forelimbs and hindlimbs, compared to their wild type littermates. Here, PRKAR1A is linked to chondrodysplasia.