Among the varied causes of craniosynostosis (premature fusion of one or more sutures of the skull vault), a monogenic etiology is most commonly identified in individuals with fusion of the coronal sutures, the major pair of transverse sutures crossing the vertex of the skull.1 Coronal synostosis, which can be present bilaterally (bicoronal) or unilaterally (unicoronal), affects approximately 1 in 10,000 children2 and is the type most commonly associated with an identifiable syndrome. Common monogenic disorders that characteristically present with coronal synostosis are Muenke (MIM: 602849) and Apert (MIM: 101200) syndromes, caused by localized gain-of-function mutations encoded by FGFR3 (MIM: 134934) and FGFR2 (MIM: 176943), respectively; Saethre-Chotzen syndrome (MIM: 101400) (TWIST1 [MIM: 601622] haploinsufficiency); TCF12-related craniosynostosis (MIM: 600480 and 615314) (also a haploinsufficiency); and craniofrontonasal syndrome (MIM: 304110) (cellular interference involving variants in the X-linked EFNB1 gene [MIM: 300035]).3,4