The persistent osteopenia and reduced bone formation in Gfra2−/− mice despite the increased osteoprogenitors suggested a defect in the orchestration of surface bone formation, which is normally achieved through the fine control of OB activity and recruitment by the network of mineral-embedded osteocytes (retired OBs); the osteocyte syncytium fulfills this role in controlling surface activity via connected dendrites networked within billions of fine canaliculi (Robling and Bonewald, 2020). This evidence concerns the gene GFRA2 and Osteopenia.