Over longer time courses, EPO has been implicated in stimulating marrow FGF23 production.41–43 These findings were also consistent with our prior studies demonstrating that mice with late osteoblast/osteocyte deletion of flox-Fgf23 in the context of CKD also had lower circulating FGF23 concentrations.31 These mice also manifested elevated serum phosphate and hyperparathyroidism demonstrating key roles for the osteocyte in FGF23-mediated skeletal disease. This evidence concerns the gene EPO and bone disorder.