McCune-Albright syndrome is a rare, genetic, non-inherited condition that causes bone tumors, bone deformity and fractures. The manifestations of MAS in each individual depend upon the extent and distribution of abnormal cells. Abnormal and prolonged activation of multiple peripheral endocrine glands occurs even while the necessary stimulatory pituitary hormones may be absent. Precocious puberty, with onset of breast development, pubic hair, and the onset of menses as early as the first few months of life may occur in females. Other manifestations include acromegaly, hyperthyroidism, hyperprolactinemia, and others. Peer review refers to the work done during the screening of submitted manuscripts and funding applications. This process encourages authors to meet the accepted standards of their discipline and reduces the dissemination of irrelevant findings, unwarranted claims, unacceptable interpretations, and personal views. Publications that have not undergone peer review are likely to be regarded with suspicion by academic scholars and professionals. McCune-Albright syndrome (MAS) is classically defined by the clinical triad of fibrous dysplasia of bone (FD), café-au-lait skin spots, and precocious puberty (PP). It is a rare disease with estimated prevalence between 1/100,000 and 1/1,000,000. FD can involve a single or multiple skeletal sites and presents with a limp and/or pain, and, occasionally, a pathologic fracture. Scoliosis is common and may be progressive. In addition to PP (vaginal bleeding or spotting and development of breast tissue in girls, testicular and penile enlargement and precocious sexual behavior in boys), other hyperfunctioning endocrinopathies may be involved including hyperthyroidism, growth hormone excess, Cushing syndrome, and renal phosphate wasting. Café-au-lait spots usually appear in the neonatal period, but it is most often PP or FD that brings the child to medical attention. Renal involvement is seen in approximately 50% of the patients with MAS. The disease results from somatic mutations of the GNAS gene, specifically mutations in the cAMP regulating protein, Gs alpha. The extent of the disease is determined by the proliferation, migration and survival of the cell in which the mutation spontaneously occurs during embryonic development.

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