Importantly, gain-of function coding variants in RUNX2 were reported in patients with midline craniosynostosis and the RUNX2 p.Ala84-Ala89del variant was reported to be significantly enriched in sagittal NCS, implicating overexpression of this gene in the etiology of craniosynsotosis102. Here, RUNX2 is linked to craniosynostosis.