Indeed, from these findings and from the evidence for a soft pliant zone of peripheral unmineralized matrix at the osteocyte lacunar wall rich in mineralization-inhibiting OPN1(Figure 2B)—rather than the OPN-rich, clearly defined thin organic coating known as the lamina limitans found in normal bone1,77—we propose that the defective mineralization of the POLs is a result of local inhibitors of mineralization that occupy an upstream role in modulating the FGF23 levels responsible for renal phosphate wasting in the XLH condition. The gene discussed is FGF23; the disease is X-linked dominant hypophosphatemic rickets.