Heterozygous Gsα-inactivating mutations lead to obesity in patients with pseudohypoparathyroidism type 1A (PHP1A) (16) and in mice (17), but only when the mutation is on the maternal allele due to tissue-specific imprinting of GNAS/Gnas, the gene encoding Gsα. This evidence concerns the gene GNAS and obesity due to melanocortin 4 receptor deficiency.