This idea that osteoblasts in fibrous dysplasia lesions may have reacquired the characteristics of a perinatal osteoblast correlates with suggestions that fibrous dysplasia may be a stem cell disease.(37) Furthermore, a non-cell autonomous mechanism may contribute to the development of fibrous dysplasia lesions(38) and may similarly modify the osteoblast response to Rs1-mediated Gs activation in an age-dependent manner. This evidence concerns the gene RS1 and fibrous dysplasia.