FGF23 (fibroblast growth factor 23) is named by 3 disorder entries.
The pinned ai-gene-review ingest carries 0 core-function terms for FGF23; the upstream review (endocrine phosphaturic hormone acting through FGFR1c and alpha-Klotho) is now complete and will appear after the next ingest refresh.
Hyperphosphatemic Familial Tumoral Calcinosis types FGF23 as causative with germline variants, on the node Biallelic FGF23 Missense Variants Blocking Intact Hormone Secretion.
Autosomal Recessive Hypophosphatemic Rickets 1; and Raine Syndrome name FGF23 only on mechanism nodes, as the hormone whose excess drives phosphate wasting: Increased Osteocytic FGF23 Production and Dysregulated FGF23 and Renal Phosphate Wasting. That is the expected shape: FGF23 is not the mutated gene in either disease.
Underlined values are claims re-computed from the knowledge base each time this page is built. The tables below are the source of truth.
Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.
| Disorder | Relationship | Where the gene appears |
|---|---|---|
| Hyperphosphatemic Familial Tumoral Calcinosis | causative germline loss of function |
mechanism: Biallelic FGF23 Missense Variants Blocking Intact Hormone Secretion
subtype: HFTC2
scoped to subtype: HFTC2
|
| Autosomal Recessive Hypophosphatemic Rickets 1 | no genetic record |
mechanism: Increased Osteocytic FGF23 Production
|
| Hereditary Hypophosphatemic Rickets with Hypercalciuria | no genetic record |
mechanism: FGF23-Independent Calcitriol Elevation
|
| Raine Syndrome | no genetic record |
mechanism: Dysregulated FGF23 and Renal Phosphate Wasting
|
Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.