FGF23 is a bone-derived hormone that regulates phosphate homeostasis by acting on the kidney to increase phosphate excretion and inhibit vitamin D synthesis. It signals through FGF receptors (FGFRs) in the presence of the coreceptor Klotho. This study identifies the parathyroid as a new target organ for FGF23 in rats. The parathyroid expresses Klotho and two FGFRs, and FGF23 increases Klotho levels and activates the MAPK pathway, leading to decreased parathyroid hormone (PTH) secretion and gene expression. In vivo and in vitro experiments show that FGF23 suppresses PTH secretion and gene expression, with the MAPK pathway playing a key role. These findings suggest that FGF23 acts directly on the parathyroid to decrease serum PTH, adding a new dimension to the understanding of mineral homeostasis. The parathyroid is thus a new target organ for FGF23, highlighting the importance of the bone-parathyroid endocrine axis in phosphorus homeostasis.FGF23 is a bone-derived hormone that regulates phosphate homeostasis by acting on the kidney to increase phosphate excretion and inhibit vitamin D synthesis. It signals through FGF receptors (FGFRs) in the presence of the coreceptor Klotho. This study identifies the parathyroid as a new target organ for FGF23 in rats. The parathyroid expresses Klotho and two FGFRs, and FGF23 increases Klotho levels and activates the MAPK pathway, leading to decreased parathyroid hormone (PTH) secretion and gene expression. In vivo and in vitro experiments show that FGF23 suppresses PTH secretion and gene expression, with the MAPK pathway playing a key role. These findings suggest that FGF23 acts directly on the parathyroid to decrease serum PTH, adding a new dimension to the understanding of mineral homeostasis. The parathyroid is thus a new target organ for FGF23, highlighting the importance of the bone-parathyroid endocrine axis in phosphorus homeostasis.