ArticleGenome biology2025
Potential synthetic associations created by epistasis.
Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- JanusX: an integrated and high-performance platform for scalable genome-wide association studies and genomic selection.The Plant journal : for cell and molecular biology · 2026Article
- Genome-wide association study reveals genomic regions associated withFrontiers in plant science · 2026Article
- Complexity welcome: Pangenome graphs for comprehensive population genomics.Quantitative plant biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The prevalence of synthetic associations in GWAS, where non-causal variants become significant by tagging multiple undetected causal variants and not necessarily in strong linkage disequilibrium with any single one, remains unexplored. We introduce a novel machine-learning approach using only genotype data to infer such associations in human GWAS. Our analysis reveals that 3-5% of GWAS Catalog peaks may represent potential synthetic associations, often arising from epistatic interactions between common variants rather than multiple rare variants acting independently. Our findings highlight the need for multi-locus models and emphasize careful GWAS interpretation and follow-up analyses like fine-mapping and trait prediction.
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Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.