What you carry at this position in your DNA and what research says about it.
Autoimmune Disease Risk: 8/10 evidence, 18 publications.
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Sample genotype (not yours): G/G
Higher Psoriasis Risk but Better Drug Response
This genotype is linked to an increased risk of developing psoriasis and psoriatic arthritis. However, it also predicts a significantly better response to TNF-inhibitor medications.
What this genotype means: Increased risk of psoriasis; Increased risk of psoriatic arthritis; Better response to TNF inhibitors.
Sample genotype (not yours): G/T
Moderately Increased Psoriasis Risk
Carrying one copy of the G allele moderately increases the risk of psoriasis and psoriatic arthritis while offering a favorable response to TNF inhibitors.
What this genotype means: Moderately increased risk of psoriasis; Slightly increased risk of psoriatic arthritis; Favorable response to TNF inhibitors.
Sample genotype (not yours): T/T
Typical Psoriasis Risk but Higher Lupus Susceptibility
This genotype is associated with a lower risk of psoriasis and psoriatic arthritis, but carries a higher susceptibility to systemic lupus erythematosus.
What this genotype means: Lower risk of psoriasis; Lower risk of psoriatic arthritis; Higher risk of systemic lupus erythematosus.
Gene function and biological role
Gene Function: The TNFAIP3 gene encodes a protein called A20, which acts as a critical negative regulator of the NF-kappaB signaling pathway [1]. By inhibiting this pathway, A20 helps shut down inflammatory responses and prevents the immune system from attacking the body's own tissues [1]. When TNFAIP3 function is altered, uncontrolled inflammation can lead to various autoimmune conditions [2]. This gene is highly expressed in immune cells and skin cells, where it plays a protective role against inflammatory damage [2].
Variant Impact: The rs610604 variant is an intron variant located within the TNFAIP3 gene that modulates its expression levels [1]. The G allele of this variant is associated with altered recruitment of regulatory proteins, leading to reduced expression of the protective A20 protein [3]. This reduction in A20 expression permits sustained inflammatory signaling, particularly in skin cells [3]. Consequently, this genetic change influences susceptibility to chronic inflammatory diseases and response to targeted biologic therapies [4].
Key Insight: The same genetic variant that increases your risk for psoriasis also makes you more likely to respond exceptionally well to certain biologic therapies like TNF inhibitors.
Location: TNFAIP3. Chromosome 6 · 6q23.3 · 137.9 Mb
Estimated prevalence by population
Global 19.2%; European 10.6%; African 40.3%; East Asian 1.1%; South Asian 9.6%; Americas 16.0%; Ashkenazi 15.2%; Finnish 11.3%; Middle Eastern 15.0%; Amish 16.1%.
Estimated GG genotype frequency.
Global 44.3%; European 43.9%; African 46.4%; East Asian 18.7%; South Asian 42.8%; Americas 48.0%; Ashkenazi 47.6%; Finnish 44.6%; Middle Eastern 47.5%; Amish 48.1%.
Estimated GT genotype frequency.
Global 36.6%; European 45.6%; African 13.4%; East Asian 80.2%; South Asian 47.7%; Americas 36.0%; Ashkenazi 37.3%; Finnish 44.1%; Middle Eastern 37.5%; Amish 35.8%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Organ Systems
Skin & Hair Conditions
Psoriasis. Evidence: 8/10. Source: PMID 19169254. Increased Risk.
Immunity & Inflammation
Autoimmune Diseases
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 35507331. ~1.15x Risk.
Lupus. Evidence: 6/10. Source: PMID 36750564. Typical Risk.
Pharmacogenomics
Immunosuppressant & Biologic Response
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 30653751. Stronger Response.
Tildrakizumab Response. Evidence: 5/10. Source: PMID 39081053. Poorer Response.
Showing effects for G/T genotype
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 35507331. Slightly Increased.
Lupus. Evidence: 6/10. Source: PMID 36750564. Slightly Increased.
Tildrakizumab Response. Evidence: 5/10. Source: PMID 39081053. Typical Response.
Showing effects for T/T genotype
Psoriasis. Evidence: 8/10. Source: PMID 19169254. Typical Risk.
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 35507331. Typical Risk.
Lupus. Evidence: 6/10. Source: PMID 36750564. Increased Risk.
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 30653751. Poorer Response.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele is associated with a higher susceptibility to psoriasis and a greater likelihood of severe symptoms [1]. This genetic variant reduces the expression of the TNFAIP3 gene, which normally acts to suppress inflammatory pathways in the skin [1]. Interestingly, while this leads to a higher risk of psoriatic arthritis [2], it also makes the inflammatory process highly dependent on TNF-alpha signaling. As a result, individuals with this genotype show a significantly better clinical response to TNF-inhibitor drugs like etanercept [3]. Conversely, they may have a poorer response to other biologics such as tildrakizumab [4]. On the positive side, this genotype is associated with a lower risk of developing systemic lupus erythematosus [5].
Increased risk of psoriasis; Increased risk of psoriatic arthritis; Better response to TNF inhibitors; Lower response to tildrakizumab.
Sample genotype: GT (Heterozygous)
Having one copy of the G allele and one copy of the T allele represents an intermediate genetic profile for autoimmune risk. This genotype is associated with a moderately increased risk of developing psoriasis and psoriatic arthritis compared to the typical baseline [1]. The presence of the G allele slightly reduces the expression of the anti-inflammatory A20 protein, leading to mild elevations in inflammatory signaling [2]. On the clinical side, individuals with this genotype still tend to respond well to TNF-inhibitor therapies [3]. They also maintain a balanced risk profile for systemic lupus erythematosus, as they carry one copy of the T allele which is associated with lupus susceptibility [4].
Moderately increased risk of psoriasis; Slightly increased risk of psoriatic arthritis; Favorable response to TNF inhibitors.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele is protective against the development of psoriasis and psoriatic arthritis [1]. Because this genotype does not experience the reduced TNFAIP3 expression caused by the G allele, skin inflammation pathways remain normally regulated [2]. However, this genotype is associated with a higher risk of developing systemic lupus erythematosus [3]. Additionally, if psoriasis does develop, individuals with this genotype may have a poorer response to TNF-inhibitor medications [4]. They may, however, respond normally or better to alternative biologic therapies like tildrakizumab [5].
Lower risk of psoriasis; Lower risk of psoriatic arthritis; Higher risk of systemic lupus erythematosus; Poorer response to TNF inhibitors.
Variants with shared genetic architecture
rs2230926 · TNFAIP3 Gene · Chr 6 · Autoimmune Disease Risk
rs582757 · TNFAIP3 Gene · Chr 6 · Psoriasis Risk
rs6920220 · TNFAIP3 Gene · Chr 6 · Rheumatoid Arthritis Risk
Genome-wide association scan yields new insights into the immunopathogenesis of psoriasis.
TNFAIP3 gene polymorphisms are associated with response to TNF blockade in psoriasis.
Content updated August 2026.
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