What you carry at this position in your DNA and what research says about it.
Rheumatoid Arthritis Risk: 6/10 evidence, 39 publications.
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Sample genotype (not yours): G/G
Higher Rheumatoid Arthritis Risk
Two copies of the G allele are associated with a significantly increased risk of developing rheumatoid arthritis and a less favorable response to common biologic therapies. This genetic profile is also linked to a higher risk of other autoimmune conditions like lupus.
What this genotype means: Elevated risk of rheumatoid arthritis; Increased risk of systemic lupus erythematosus; Reduced response to TNF-alpha inhibitors.
Sample genotype (not yours): A/A
Typical Rheumatoid Arthritis Risk
Two copies of the A allele represent the typical genetic baseline, carrying no elevated risk for rheumatoid arthritis or lupus. This profile is also associated with a standard response to biologic therapies.
What this genotype means: Typical baseline risk for rheumatoid arthritis; Standard response to TNF-alpha inhibitors; Typical baseline risk for lupus.
Sample genotype (not yours): G/A
Increased Rheumatoid Arthritis Risk
One copy of the G allele is linked to an elevated risk of developing rheumatoid arthritis. This genotype may also reduce the effectiveness of certain biologic medications used to treat joint inflammation.
What this genotype means: Elevated risk of rheumatoid arthritis; Slightly increased risk of systemic lupus erythematosus; Potentially reduced response to TNF-alpha inhibitors.
Gene function and biological role
Gene Function: The TRAF1 gene encodes tumor necrosis factor receptor-associated factor 1, a key regulator of inflammation and cell survival [1]. It plays a critical role in mediating signals from various TNF family receptors, which are central to the body's immune response [2]. Dysregulation of this pathway is heavily implicated in the pathogenesis of autoimmune disorders [3]. Specifically, the protein helps control programmed cell death and the activation of inflammatory transcription factors [4].
Variant Impact: Located in the first intron of the TRAF1 gene, rs3761847 is a single nucleotide polymorphism that influences gene expression in immune cells [1]. The genetic variation alters the regulation of the TRAF1-C5 locus, which is a well-established susceptibility region for chronic inflammatory conditions [5]. Research indicates that the G allele at this position is associated with a heightened inflammatory state and increased susceptibility to autoimmune diseases [6]. Conversely, the A allele is linked to typical immune regulation and a lower likelihood of developing these conditions [7].
Key Insight: While the G allele increases the risk of rheumatoid arthritis, it is also associated with a significantly higher risk of mortality from severe infections and cancers in those who develop the disease, highlighting its broad impact on immune system regulation.
Location: TRAF1. Chromosome 9 · 9q33.2 · 120.9 Mb
Estimated prevalence by population
Global 22.9%; European 18.9%; African 35.4%; East Asian 22.7%; South Asian 8.9%; Americas 16.0%; Ashkenazi 11.3%; Finnish 20.9%; Middle Eastern 10.4%; Amish 29.7%.
Estimated GG genotype frequency.
Global 48.5%; European 49.1%; African 48.2%; East Asian 49.9%; South Asian 41.8%; Americas 48.0%; Ashkenazi 44.7%; Finnish 49.6%; Middle Eastern 43.7%; Amish 49.6%.
Estimated GA genotype frequency.
Global 28.6%; European 32.0%; African 16.4%; East Asian 27.5%; South Asian 49.3%; Americas 36.0%; Ashkenazi 44.0%; Finnish 29.5%; Middle Eastern 45.8%; Amish 20.7%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 6/10. Source: PMID 17804836. ~1.3x Risk.
Lupus. Evidence: 6/10. Source: PMID 36750564. Increased Risk.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Lymphocyte Count. Evidence: 6/10. Source: PMID 39024449. Typical.
Pharmacogenomics
Immunosuppressant & Biologic Response
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 25834819. Poorer Response.
Showing effects for A/A genotype
Rheumatoid Arthritis. Evidence: 6/10. Source: PMID 17804836. Typical Risk.
Lupus. Evidence: 6/10. Source: PMID 36750564. Typical Risk.
Lymphocyte Count. Evidence: 6/10. Source: PMID 39024449. Slightly Higher.
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 25834819. Typical Response.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
A double dose of the G allele at this locus is a well-documented genetic risk factor for rheumatoid arthritis, particularly the anti-CCP positive subtype [1]. Studies show that this genotype increases the odds of developing the condition by more than 1.3 times compared to the typical baseline [2]. Furthermore, in patients who already have rheumatoid arthritis, this genetic profile is associated with increased overall mortality, primarily driven by a higher susceptibility to severe infections and malignancies rather than cardiovascular issues [3]. It is also linked to a higher risk of systemic lupus erythematosus [4]. Additionally, clinical research indicates that people with this genotype may experience a poorer response to tumor necrosis factor alpha inhibitors, which are commonly prescribed biologic treatments [5].
Elevated risk of rheumatoid arthritis; Increased risk of systemic lupus erythematosus; Reduced response to TNF-alpha inhibitors.
Sample genotype: AA (Homozygous)
The presence of two A alleles represents the standard genetic baseline for this locus, carrying no elevated risk for rheumatoid arthritis [1]. Research indicates that this genotype is associated with a typical, healthy immune response and does not predispose to systemic lupus erythematosus. In patients diagnosed with rheumatoid arthritis, this profile is linked to a more favorable long-term survival outlook compared to those carrying the G allele [2]. Furthermore, individuals with this genotype tend to show a standard, more effective response to tumor necrosis factor alpha inhibitors when treated for inflammatory conditions [3]. Additionally, this genetic profile is associated with slightly higher typical lymphocyte counts in the blood [4].
Typical baseline risk for rheumatoid arthritis; Standard response to TNF-alpha inhibitors; Typical baseline risk for lupus.
Sample genotype: GA (Heterozygous)
Inheriting one G allele and one A allele is associated with a moderately increased risk of developing rheumatoid arthritis [1]. Large-scale genetic studies estimate that this heterozygous profile carries approximately 1.3 times the risk of the typical baseline [2]. The risk is particularly pronounced for anti-CCP antibody-positive and rheumatoid factor-positive forms of the disease [3]. This genetic variation is also associated with a slightly elevated risk of systemic lupus erythematosus [4]. In terms of treatment, clinical evidence suggests that individuals with this genotype may have a less optimal response to TNF-alpha inhibitor therapies [5].
Elevated risk of rheumatoid arthritis; Slightly increased risk of systemic lupus erythematosus; Potentially reduced response to TNF-alpha inhibitors.
Variants with shared genetic architecture
rs7097397 · WDFY4 Gene · Chr 10 · Autoimmune Disease Risk
rs8032939 · RASGRP1 Gene · Chr 15 · Rheumatoid Arthritis Risk
rs1234313 · TNFSF4 Gene · Chr 1 · Autoimmune Disease Risk
TRAF1-C5 as a risk locus for rheumatoid arthritis--a genomewide study.
Rheumatoid arthritis: a view of the current genetic landscape.
Genetics of rheumatic disease.
Susceptibility variants for rheumatoid arthritis in the TRAF1-C5 and 6q23 loci: a meta-analysis.
Genome-wide association study meta-analysis identifies seven new rheumatoid arthritis risk loci.
TRAF1 polymorphisms associated with rheumatoid arthritis susceptibility in Asians and in Caucasians.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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