When heterozygous mutations are located in the maternal allele of GNAS exons 1–13, patients exhibited multiple hormone resistance, which act via the Gs-coupled receptors such as parathyroid hormone (PTH), thyroid-stimulating hormone (TSH), gonadotropins, growth hormone-releasing hormone (GHRH), in addition to the more traditional AHO features. Here, PTH is linked to pseudohypoparathyroidism type 1A.