Links from this page to related variants, conditions, drugs and topics are not included for automated readers. Those connections are the Gene Knowledge Graph and are licensed as data: https://www.mygenelog.com/license
EIF2AK3 · rs6739095
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
Its strongest genetic-study result is p = 10−54, with 1 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 360,388 European ancestry individuals, 165,056 East Asian ancestry individuals.
The effect Each copy of the A allele shifted the measure 0.0204 lower (95% confidence interval 0.018-0.023); p = 3 × 10−54.
Where it sits Chromosome 2, band 2p11.2 — in an intron of EIF2AK3.
How common each version is
AT
A 53.0% · T 47.0%
A 54.3% · T 45.7%
A 55.6% · T 44.4%
A 56.7% · T 43.3%
A 45.8% · T 54.2%
A 70.3% · T 29.7%
A 64.9% · T 35.1%
A 71.4% · T 28.6%
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.
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
Height (rs6739095). MyGeneLog™. https://www.mygenelog.com/variants/rs6739095