Consistent with the established functions of DMP1, short-term pharmacologic administration and long-term osseous overexpression of DMP1 also correct FGF23 elevations in 129 Sv and B6 Col4a3−/− mice, independently of kidney disease progression and circulating levels of calcium or PTH, and despite worsening of hyperphosphatemia. The gene discussed is PTH; the disease is hyperphosphatemia.