In other tissues, no imprinting would be expected and a 50% reduction of Gsα activity is still sufficient for maintaining normal signaling activity in most cells but leads to haploinsufficiency in others tissues involved in the AHO phenotype, such as the growth plate.[14] Many PHP-1a and PPHP patients have a similar heterozygous loss-of-function mutation in the GNAS gene; however, the severity of AHO is variable. The gene discussed is GNAS; the disease is pseudopseudohypoparathyroidism.