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WNT10A · rs121908120
Stands on its own. Nothing else here links to this position yet — but the page above is the point: what the research found, what each genotype means, and where it came from, in language you can read. Links to conditions, drugs and the senses appear automatically if we write them.
Strength of the evidence
ClinVar classifies it as disease-causing (or likely), reviewed at 2 of 4 stars. Its strongest genetic-study result is p = 10−46, with 17 associations in the GWAS Catalog.
4: ClinVar disease-causing, reviewed by an expert panel or a guideline (3–4 stars). 3: ClinVar, several labs agreeing (2 stars), or a genetic study at p ≤ 10−50. 2: ClinVar from one lab (1 star), or p ≤ 10−20. 1: ClinVar submitted without criteria (0 stars), or genome-wide significance (p ≤ 5×10−8). The higher of the two counts. It says how solid the evidence is, not whether it matters for a particular person.
What the study found
Who was studied 1,944 Icelandic ancestry cases, 338,554 Icelandic ancestry controls (includes non-array genotyped, whole-genome imputed individuals); replicated in 151 European ancestry cases, 6,019 European ancestry controls, 150 European and other ancestry cases, 2,696 European and other ancestry controls.
The effect Each copy of the A allele carried 3.25 times the odds of Tooth agenesis (95% confidence interval 2.74-3.85); p = 2 × 10−40.
How common The A allele had a frequency of about 3% in the people studied.
Where it sits Chromosome 2, band 2q35 — a missense change in WNT10A.
What ClinVar records
Classification
Pathogenic/Likely pathogenic/Pathogenic, low penetrance for Odonto-onycho-dermal dysplasia, Tooth agenesis, selective, 4, Inborn genetic diseases, Hypohidrotic ectodermal dysplasia, Tooth agenesis and 5 more; criteria provided, multiple submitters, no conflicts (2 of 4 stars, 44 submitters), last evaluated 2026-09-01.
ClinVar record 4462 NM_025216.3(WNT10A):c.682T>A (p.Phe228Ile)
Change history MyGeneLog™ keeps a copy of every weekly release from 2026-10-19 and compares them. This position's classification has not changed since.
What this is ClinVar's aggregate record for this position (as of its 2026-11-09 release), not a result about you. A classification describes the variant against the condition named, as laboratories submitted it. Whether a person carries this variant, and what that would mean for them, is a question for a clinical test and a genetic counsellor.
How common each version is
AT
A 1.4% · T 98.6%
A 0.6% · T 99.4%
A 1.5% · T 98.5%
By ancestry gnomAD
A 2.2% · T 97.8%
T 99.6%
T 99.8%
A 1.6% · T 98.4%
A 2.7% · T 97.3%
T 99.6%
A 3.5% · T 96.5%
The share of all copies of this position that are each version. Source: the population studies published in dbSNP (US NCBI); each row names its study. The ancestry rows are gnomAD's own groups (via Ensembl), as the survey defines them, not races. No Korean figure for this position yet.
2026-06-04 · Nam K et al., Nature Communications 2026 (PMID 42243103)
Your Mouth and the Rest of Your Body: Genes Behind 21 Mouth and Face Diseases
A UK Biobank study looked at the genetics of 21 diseases of the mouth and face together and found 48 new places in the genome. For gum disease (periodontitis), a change in ALDH1A2, a gene that makes retinoic acid, lowered how much protein the gene produced, and gum tissue from patients showed weaker retinoic acid signalling. Tooth decay and gum disease shared a lot of genetics with diseases elsewhere in the body, but without clear cause and effect; for Sjögren’s syndrome, the analysis supported a causal link with lung cancer and stroke. Positions with pages here include rs121908120 in WNT10A (tooth decay) and rs11084095 in SIGLEC5 (gum disease).
Licensed CC BY-NC 4.0: free to read, share and adapt for non-commercial use, naming MyGeneLog™ and linking the exact page. Commercial use, including training or serving a commercial AI system, needs a licence — https://www.mygenelog.com/license
Tooth agenesis (rs121908120). MyGeneLog™. https://www.mygenelog.com/variants/rs121908120