ReviewCell2017
An Expanded View of Complex Traits: From Polygenic to Omnigenic.
Review in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04331535 (Pragmatic Randomized Trial of Polygenic Risk Scoring for Common Diseases in Primary Care), which is not on this map. Cited by 1,581 papers, 1 of them a synthesis that pooled it.
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.
Pragmatic Randomized Trial of Polygenic Risk Scoring for Common Diseases in Primary Care
Who cites it
1,581 citing papers in PubMed, 1 synthesis or guideline pooled it, 3,117 citations in OpenAlex.
- Genetic drivers of etiologic heterogeneity in thyroid cancer.Nature communications · 2026Pooled it
- The role ofEpigenetics · 2026Review
- Signatures of selection in pleiotropic genes involved in insect neuronal and immune systems.G3 (Bethesda, Md.) · 2026Article
- Translating functional molecular knowledge into crop-breeding success.Nature reviews. Genetics · 2026Review
- A heritability-optimized method for functional prioritization of rare coding variants in complex traits.Nature genetics · 2026Article
- Genetic landscape of an in vivo protein interactome.Nature genetics · 2026Article
- Article
- Polygenic risk scores and plasma proteomics identify cancer-related proteins and trans-regulated protein networks.Cell genomics · 2026Article
- Genetic architectures of brain-related traits are shaped by strong selective constraints.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enhancing detection of polygenic adaptation: a comparative study of machine learning and statistical approaches using simulated evolve-and-resequence data.BMC genomics · 2026Article
- Polygenic and monogenic adaptation drive evolutionary rescue at different magnitudes of environmental change.The Journal of heredity · 2026Article
- Article
- Allele frequencies at recessive disease genes are mainly determined by pleiotropic effects in heterozygotes.Genetics · 2026Article
- Scale-Invariant, Robust Sparse PCA for Large Data via Differentiable Penalties.Transactions on machine learning research · 2026Article
- Article
- Cell-type specific analyses in blood and gut identify cis-eQTL matching 140 IBD risk loci and entrectinib as repurposing candidate.Nature communications · 2026Article
- The Omnicausal Model Reveals the Highly Polyfactorial Nature of Complex Diseases.Genetic epidemiology · 2026Article
- Robust Inference With Ghostknockoffs in Genome-Wide Association Studies With Sample Relatedness.Genetic epidemiology · 2026Article
- Gene-level complexity explains genome-wide variation in the distribution of fitness effects.Molecular biology and evolution · 2026Article
- Article
1,521 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
A central goal of genetics is to understand the links between genetic variation and disease. Intuitively, one might expect disease-causing variants to cluster into key pathways that drive disease etiology. But for complex traits, association signals tend to be spread across most of the genome-including near many genes without an obvious connection to disease. We propose that gene regulatory networks are sufficiently interconnected such that all genes expressed in disease-relevant cells are liable to affect the functions of core disease-related genes and that most heritability can be explained by effects on genes outside core pathways. We refer to this hypothesis as an "omnigenic" model.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.