However, finding that the brittleness of A/J femurs was not improved following Scl-Ab treatment is consistent with the work of others [9, 12] which showed Brtl/+ mice (Type IV osteogenesis imperfecta (OI) model) treated with a sclerostin antibody failed to significantly improve tissue ductility. The gene discussed is SOST; the disease is osteogenesis imperfecta.