Effect of systemic Celecoxib therapy in both human FD cells and mouse FDLL caused by Prkar1a deficiency. In vitro and in vivo Celecoxib treatment led to decreased proliferation of FD cells and FDLLs. Celecoxib treatment in mice improved the histologic phenotype and cortical bone organization of FDLLs associated with Prkar1a deficiency. This study presents promising results for the treatment of mice with bone lesions caused by Prkar1a deficiency. Potential role of Celecoxib in the treatment of patients with FD or CNC; however, to date no such human trail has been conducted.