SCN9A

Chr 2ADAR

sodium voltage-gated channel alpha subunit 9

Also known as: ETHA, FEB3B, GEFSP7, HSAN2D, NE-NA, NENA, Nav1.7, PN1

This gene encodes a voltage-gated sodium channel that mediates nociception signaling in peripheral sensory neurons. Mutations cause a spectrum of pain disorders including primary erythermalgia, paroxysmal extreme pain disorder, congenital insensitivity to pain, and small fiber neuropathy, typically through gain-of-function mechanisms that alter channel activity. Inheritance is autosomal dominant for most pain disorders, though some forms show autosomal recessive inheritance.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
GOFmechanismAD/ARLOEUF 0.715 OMIM phenotypes
Clinical SummarySCN9A
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Gene-Disease Validity (ClinGen)
epilepsy · ADRefuted

Refuted — evidence has disproved this relationship

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
30 unique Pathogenic / Likely Pathogenic· 308 VUS of 500 total submissions
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — SCN9A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.71LOEUF
pLI 0.000
Z-score 3.70
OE 0.55 (0.430.71)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.06Z-score
OE missense 0.91 (0.860.96)
913 obs / 1007.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.55 (0.430.71)
00.351.4
Missense OE0.91 (0.860.96)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 43 / 78.3Missense obs/exp: 913 / 1007.5Syn Z: -1.08
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveSCN9A-related erythromelalgia, primaryGOFAD
DN
0.83top 10%
GOF
0.87top 5%
LOF
0.1994th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median · 1 literature citation
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

GOFThese data do not correlate with the clinical picture of our case and her father, but intra- and interfamily phenotypic diversity in symptoms associated with a gain-of-function variant of Na(V)1.7 are also described and may explain our case.PMID:24817410

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic20
Likely Pathogenic10
VUS308
Likely Benign147
Benign1
20
Pathogenic
10
Likely Pathogenic
308
VUS
147
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
17
2
1
0
20
Likely Pathogenic
8
2
0
0
10
VUS
4
288
12
4
308
Likely Benign
0
1
52
94
147
Benign
0
0
1
0
1
Total292936698486

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

SCN9A · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
The Evolving Landscape of Small Fiber Neuropathy.
Devigili G et al.·Semin Neurol
2025Review
Erythromelalgia.
Klein-Weigel PF et al.·Vasa
2018Review
Small fibre neuropathy.
Cazzato D et al.·Curr Opin Neurol
2017Review
Top 5 results · since 2015Search PubMed ↗