MAS is characterized by the triad of monostotic/polyostotic fibrous dysplasia (FD), café au lait skin pigmentation, and hyperfunctioning endocrinopathies, including gonadotropin-independent precocious puberty (PP), thyrotoxicosis, growth hormone (GH) excess, hyperprolactinemia, or neonatal hypercortisolism (2–6). The gene discussed is GH1; the disease is polyostotic fibrous dysplasia.