This study involving patients in whom hemodialysis was being initiated shows that increased levels of fibroblast growth factor 23 (FGF-23), a hormone that enhances the renal excretion of phosphate, appear to be independently associated with mortality. Whether FGF-23 is a potential biomarker that could guide strategies to reduce phosphorus levels in patients with chronic kidney disease remains to be established. This study involving patients in whom hemodialysis was being initiated shows that increased levels of fibroblast growth factor 23 (FGF-23) appear to be independently associated with mortality. Fibroblast growth factor 23 (FGF-23), a hormone that is secreted by osteoblasts, is an important regulator of phosphorus and vitamin D metabolism. It was first described as a pathogenic factor in rare hypophosphatemic syndromes in which “primary” increases in biologically active FGF-23 cause renal phosphate wasting, hypophosphatemia, inappropriately low levels of 1,25-dihydroxyvitamin D, and rickets or osteomalacia. 1 – 5 In contrast, depletion of FGF-23 leads to hyperphosphatemia, excessive levels of 1,25-dihydroxyvitamin D, ectopic calcification, and early death. 6 – 8 Subsequent studies highlighted the physiologic role of FGF-23 in maintaining normal serum phosphate levels despite variability in dietary phosphorus intake. 9 , 10 In patients . . .