In mouse models that harbor gain-of-function Fgfr2 variants associated with human craniosynostosis syndromes, mechanisms of premature fusion of the coronal suture include altered proliferation and induction of ectopic osteoblast differentiation (Holmes et al., 2009; Wang et al., 2005; Yin et al., 2008; Pfaff et al., 2016; Hajihosseini et al., 2001). This evidence concerns the gene FGFR2 and craniosynostosis.