As research continued on these conditions, it became clear that the above-mentioned picture was complicated by the finding of a clinical and molecular overlap among the different PHP subtypes, as well as by the discovery of genetic defects in genes such as PRKAR1A and PDE4D associated with acrodysostosis (ACRDYS), which shares many aspects of PHP bone and endocrine phenotype [38–55]. Here, PRKAR1A is linked to acrodysostosis.