ArticleNature2026
Causal modelling of gene effects from regulators to programs to traits.
Article in Nature, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed.
- AlphaGenome Atlas:medRxiv : the preprint server for health sciences · 2026Article
- Genome-scale perturbation signatures from primary human CD4bioRxiv : the preprint server for biology · 2026Article
- Allele frequencies at recessive disease genes are mainly determined by pleiotropic effects in heterozygotes.Genetics · 2026Article
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- Artificial intelligence in drug discovery - what it is, where we stand and the path forward.Nature reviews. Drug discovery · 2026Review
- How physiology solves the gene-centric impasse.Experimental physiology · 2026Review
- Reference Regulatory Element-Guided Gene Expression Analysis for Mechanistic Inference of Gene Regulatory Networks.bioRxiv : the preprint server for biology · 2026Article
- Translating genome-wide association studies at multiple scales: Drug target prioritization, cellular architectures, and organ imaging.Cell genomics · 2026Review
- NERINE reveals rare variant associations in gene networks across phenotypes and implicates an SNCA-PRL-LRRK2 subnetwork in Parkinson's disease.Cell genomics · 2026Article
- When network biology meets human genetics.Cell genomics · 2026Article
- Causal effect estimation from trans-regulatory single-cell CRISPR screens.Cell genomics · 2026Review
- DNAwhisper: An Integrated Deep Learning Pyramidal Framework for Multi-Trait Genomic Prediction and Adaptive Marker Prioritisation.Plant biotechnology journal · 2026Article
- Vascular smooth muscle cell state trajectories mediate molecular mechanisms of coronary disease risk.Nature communications · 2026Article
- Representation in genetic studies affects inference about genetic architecture.bioRxiv : the preprint server for biology · 2026Article
- Article
- Article
- The interaction of biological network topology and mutation effects in complex trait evolution.Frontiers in systems biology · 2026Review
- Genome-Wide Aggregated Trans-Effects Analysis Implicates Deficient Type III Interferon Signaling as a Key Cause of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2025Article
- Aggregation of recount3 RNA-seq data improves inference of consensus and tissue-specific gene coexpression networks.Genome research · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Genetic association studies provide a unique tool for identifying candidate causal links from genes to human traits and diseases. However, it is challenging to determine the biological mechanisms underlying most associations, and we lack genome-scale approaches for inferring causal mechanistic pathways from genes to cellular functions to traits. Here we propose approaches to bridge this gap by combining quantitative estimates of gene-trait relationships from loss-of-function burden tests
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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.