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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
3 / 4
Its strongest genetic-study result is p = 10−89, with 4 associations in the GWAS Catalog.
How this is scored
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 2,853 European ancestry cases and 37,405 European ancestry controls; replicated in 1,827 European ancestry cases and 2,181 European ancestry controls.
The effect
The reported allele is A; the catalogue records no effect size
; p = 3 × 10−89.
How common The A allele had a frequency of about 43% in the people studied.
Where it sits Chromosome 6, band 6p21.32 — between genes, 4.7 kb from HLA-DQA1.
What each result means
A/ATwo copies of the version the research linked to Vitiligo. That is the strongest link of the three results. A link in a study is not a diagnosis.
A/TOne copy of the version the research linked to Vitiligo. That is a smaller link than two copies.
T/TNo copy of the version the research linked to Vitiligo. This is the starting point the study compared everyone against.
DNA databases also record a third, rare version at this position, carried on fewer than one in a hundred copies of the DNA. The three results above cover the two common versions only.
Nature genetics · 2016 · PMID 27723757 · open access
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