NOTCH2 and spondylocostal dysostosis: LFNG participates in the Notch signaling pathway by inhibiting the Notch ligand JAG1,(48) which is required for normal trabecular bone formation and is the most highly expressed Notch ligand during skeletal development.(49, 50) LFNG is a mediator of somite segmentation and patterning during embryogenesis and modulates Notch signaling by decreasing the binding of JAG1 to NOTCH2.(51) Mutations in LFNG have also been associated with spondylocostal dysostosis.(52)