To test a role for FGF23 in myeloma bone disease, we used the pan-FGFR tyrosine kinase inhibitor NVP-BGJ398, which rapidly normalized phosphate and enhanced bone growth - with increased mineralization and normalization of growth plate structure - in a mouse model of ADHR, where elevated FGF23 causes hypophosphatemia [47]. This evidence concerns the gene FGF23 and autosomal dominant hypophosphatemic rickets.