In preclinical models, recombinant FGF23 was found to increase parathyroid Klotho levels and activate MAPK signaling, leading to a suppression of PTH expression over short time courses.17 However, it is also noted that genetic models of hypophosphatemia due to chronic elevated FGF23, such as XLH, are associated with elevated PTH concentrations, even in the absence of phosphate treatment.18, 19 This mild secondary hyperparathyroidism may be attributable to FGF23 excess inducing a relative deficiency in 1,25(OH)2D. Here, FGF23 is linked to hypophosphatemia.