What you carry at this position in your DNA and what research says about it.
Rheumatoid Arthritis Risk: 8/10 evidence, 36 publications.
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Sample genotype (not yours): G/G
Typical Autoimmune Risk
Inheriting the common G allele from both parents is associated with baseline levels of inflammation. This genotype does not carry the elevated risk of autoimmune conditions linked to the alternative A allele.
What this genotype means: Typical risk of rheumatoid arthritis; Typical levels of systemic inflammation; Standard response to anti-TNF medications.
Sample genotype (not yours): A/A
Elevated Autoimmune Risk and Poorer Drug Response
Inheriting two copies of the A allele is associated with a higher risk of rheumatoid arthritis and other inflammatory disorders.
What this genotype means: ~1.7x higher risk of rheumatoid arthritis; Increased risk of ulcerative colitis and lupus; Potentially reduced response to anti-TNF therapies.
Sample genotype (not yours): G/A
Moderately Increased Autoimmune Risk
Presence of a single A allele is linked to a slightly higher risk of developing rheumatoid arthritis and other inflammatory conditions.
What this genotype means: ~1.2x higher risk of rheumatoid arthritis; Slightly increased risk of inflammatory bowel disease; Slightly elevated baseline inflammation markers.
Gene function and biological role
Gene Function: The TNFAIP3 gene encodes the A20 protein, a critical regulator of the body's inflammatory response [1]. A20 acts as a molecular brake on the NF-kB pathway, which prevents immune cells from overreacting to inflammatory signals [2]. Without adequate A20 function, the immune system remains in a hyper-active state, leading to chronic tissue damage [3]. Mice genetically deficient in this protein develop severe, destructive joint inflammation resembling human arthritis [3]. This gene is therefore highly studied as a central hub in the development of multiple autoimmune conditions [1].
Variant Impact: This intergenic variant is located on chromosome 6 in a region between the OLIG3 and TNFAIP3 genes [4]. It acts as a genetic marker that influences the expression and regulatory activity of the nearby TNFAIP3 gene [5]. The minor A allele is associated with altered inflammatory signaling and a higher baseline level of systemic inflammation [6]. This genetic change has been consistently linked to an increased susceptibility to several autoimmune disorders, particularly rheumatoid arthritis [4]. It also appears to affect how the body responds to certain anti-inflammatory medications [7].
Key Insight: This variant acts as a genetic volume dial for inflammation, where carrying the A allele makes the immune system more prone to attacking the body's own tissues.
Location: TNFAIP3. Chromosome 6 · 6q23.3 · 137.7 Mb
Estimated prevalence by population
Global 71.2%; European 62.7%; African 79.2%; East Asian 99.4%; South Asian 80.0%; Americas 76.5%; Ashkenazi 72.7%; Finnish 67.6%; Middle Eastern 75.8%; Amish 70.9%.
Estimated GG genotype frequency.
Global 26.0%; European 33.0%; African 19.5%; East Asian 0.6%; South Asian 18.9%; Americas 21.9%; Ashkenazi 25.1%; Finnish 29.2%; Middle Eastern 22.5%; Amish 26.6%.
Estimated GA genotype frequency.
Global 2.8%; European 4.3%; African 1.2%; East Asian < 0.1%; South Asian 1.1%; Americas 1.6%; Ashkenazi 2.2%; Finnish 3.2%; Middle Eastern 1.7%; Amish 2.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 8/10. Source: PMID 17982456. Typical Risk.
Lupus. Evidence: 3/10. Source: PMID 19838195. Typical Risk.
Chronic Inflammatory Diseases
Ulcerative Colitis. Evidence: 8/10. Source: PMID 21297633. Typical Risk.
Inflammatory & Circulating Protein Markers
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Typical Levels.
TNF-Alpha Response. Evidence: 5/10. Source: PMID 30653751. Typical Response.
Organ Systems
Liver Function & Disease
Biliary Cholangitis. Evidence: 3/10. Source: PMID 22936693. Typical Risk.
Lifestyle, Fitness & Aging
Height & Body Size
Height. Evidence: 4/10. Source: PMID 36224396. Slightly Taller.
Showing effects for A/A genotype
Rheumatoid Arthritis. Evidence: 8/10. Source: PMID 17982456. ~1.7x Increased Risk.
Lupus. Evidence: 3/10. Source: PMID 19838195. ~1.17x Increased Risk.
Ulcerative Colitis. Evidence: 8/10. Source: PMID 21297633. ~1.15x Increased Risk.
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Elevated Levels.
TNF-Alpha Response. Evidence: 5/10. Source: PMID 30653751. Poorer Response.
Biliary Cholangitis. Evidence: 3/10. Source: PMID 22936693. ~1.29x Increased Risk.
Height. Evidence: 4/10. Source: PMID 36224396. Slightly Shorter.
Showing effects for G/A genotype
Rheumatoid Arthritis. Evidence: 8/10. Source: PMID 17982456. ~1.2x Increased Risk.
Lupus. Evidence: 3/10. Source: PMID 19838195. Slightly Increased.
Ulcerative Colitis. Evidence: 8/10. Source: PMID 21297633. Slightly Increased.
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Slightly Elevated.
Biliary Cholangitis. Evidence: 3/10. Source: PMID 22936693. Slightly Increased.
Height. Evidence: 4/10. Source: PMID 36224396. Typical Height.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Standard genetic variations at this chromosome 6 locus represent the baseline profile [1]. Large-scale genome-wide association studies show that this genotype is associated with a typical risk of developing rheumatoid arthritis and other inflammatory conditions [2]. The body maintains standard regulation of the TNFAIP3 gene, which helps keep inflammatory pathways in check [3]. Standard levels of C-reactive protein, a key marker of systemic inflammation, are typical for this profile [4]. Additionally, clinical studies suggest a standard, favorable response to anti-TNF therapies if they are ever needed for inflammatory conditions [5].
Typical risk of rheumatoid arthritis; Typical levels of systemic inflammation; Standard response to anti-TNF medications.
Sample genotype: AA (Homozygous)
Two copies of the A allele significantly increase the likelihood of developing autoimmune conditions [1]. Clinical studies show that this genotype is linked to an approximate 1.7-fold increase in the risk of rheumatoid arthritis [2]. The double dose of the risk allele is thought to compromise the regulatory control of the TNFAIP3 gene, leading to less effective suppression of inflammatory pathways [3]. This can result in elevated baseline levels of C-reactive protein and a higher tendency toward chronic inflammation [4]. Furthermore, research suggests that individuals with this genotype may have a poorer response to tumor necrosis factor inhibitors, which are common biologic treatments for autoimmune diseases [5].
~1.7x higher risk of rheumatoid arthritis; Increased risk of ulcerative colitis and lupus; Potentially reduced response to anti-TNF therapies.
Sample genotype: GA (Heterozygous)
A single copy of the A allele is associated with a moderate increase in susceptibility to several autoimmune diseases [1]. Research indicates that this genotype increases the risk of developing rheumatoid arthritis by approximately 1.2 times compared to the general population [2]. This genetic change is thought to slightly reduce the efficiency of the TNFAIP3 gene's anti-inflammatory braking system [3]. As a result, baseline levels of C-reactive protein, an indicator of systemic inflammation, may be slightly higher [4]. While this represents an elevated risk, the vast majority of people with this genotype do not go on to develop an autoimmune disease, as environmental factors play a major role [5].
~1.2x higher risk of rheumatoid arthritis; Slightly increased risk of inflammatory bowel disease; Slightly elevated baseline inflammation markers.
Variants with shared genetic architecture
rs2230926 · TNFAIP3 Gene · Chr 6 · Autoimmune Disease Risk
rs582757 · TNFAIP3 Gene · Chr 6 · Psoriasis Risk
rs610604 · TNFAIP3 Gene · Chr 6 · Autoimmune Disease Risk
Two independent alleles at 6q23 associated with risk of rheumatoid arthritis.
Association of the 6q23 region with the rate of joint destruction in rheumatoid arthritis.
Genetic analysis of over half a million people characterises C-reactive protein loci.
Genetic variants in the prediction of rheumatoid arthritis.
Content updated August 2026.
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