Thus the ENU mutation resulting in Oed and Sml gives rise to a bone phenotype more in keeping with that generally associated with AHO (both PHP1A and PHPP) rather than POH, in that it is confined to superficial tissues and is attributable to haploinsufficiency of biallelically expressed Gsα. This evidence concerns the gene GNAS and pseudohypoparathyroidism type 1A.