Curated summary · agent-written · kb/genes/curated/hgnc_6344.md
All 9 claims checked against the KB draft

KL across dismech

KL (klotho) is named by 1 disorder entry. It encodes alpha-Klotho, the co-receptor that FGF23 needs to signal through FGF receptors in the kidney.

Normal function

The pinned ai-gene-review snapshot that the ingest layer reads has no core functions for KL (0 terms). An upstream review of the gene is being added or updated.

Causative records

One entry types KL as causative: Hyperphosphatemic Familial Tumoral Calcinosis, recording the variants as germline. There the gene sits on the node Biallelic KL Loss of Function and Renal FGF23 Resistance.

Where the layers disagree

The KB's nodes naming KL carry no GO process annotations (0 terms), and ClinGen classifies the gene for 0 diseases.

Underlined values are claims re-computed from the knowledge base each time this page is built. The tables below are the source of truth.

In the knowledge base · computed from kb/ at build time

Disorders

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.

DisorderRelationshipWhere the gene appears
Hyperphosphatemic Familial Tumoral Calcinosis causative germline loss of function
mechanism: Biallelic KL Loss of Function and Renal FGF23 Resistance
subtype: HFTC3
scoped to subtype: HFTC3

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.