In agreement with the notion that the CKD-induced upregulation in osteoblastic and osteocytic Fgf23 secretion contributes to the mineralization defect in CKD mice, 5/6-Nx failed to significantly suppress TNAP activity in Fgf23/VDR mice (Figure 5D), and pyrophosphate concentrations remained unchanged in bones of CKD Fgf23/VDR mice (Figure 5E). The gene discussed is VDR; the disease is chronic kidney disease.