TGFB1 and cranioectodermal dysplasia: The inadequate activation of TGF-β1 on unnecessary sites leads to poor-quality bone formation, unfilled resorbed areas, and haphazard sclerotic areas.[9] Understanding the pathophysiology of the disease provided important insights into its treatment strategies; currently, corticosteroids and angiotensin receptor II blockers are recommended to improve the clinical outcome of patients with CED.[10,11]