Mice with constitutively active PPR in osteocytes display increased trabecular bone mass, increased osteoblast number, and decreased Sost/sclerostin expression [20, 21] whereas mice lacking RANKL in osteocytes have high bone mineral density and osteopetrosis [14, 15], demonstrating an important role for osteocytes in bone remodeling. The gene discussed is SOST; the disease is osteopetrosis.