Our previous studies showed that knocking out Family with sequence similarity member 20-b (Fam20b) in mouse CNCCs also resulted in persistent potency of sutures and craniosynostosis by impairing GAG chain synthesis (Liu et al., 2018), implicating the role of GAG chains in mediating signaling activity in CNCC derived cranium. The gene discussed is FAM20B; the disease is craniosynostosis.