What you carry at this position in your DNA and what research says about it.
Gastric Cancer Risk: 5/10 evidence, 52 publications.
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Sample genotype (not yours): G/G
Typical Gastric Cancer Risk
Possessing the common G/G genotype is associated with typical baseline risks for gastric cancer and inflammatory conditions. However, there may be an increased risk of organ rejection when treated with cyclosporine after transplantation.
What this genotype means: Typical baseline risk of gastric cancer; Increased risk of cyclosporine-related organ rejection.
Sample genotype (not yours): A/A
Significantly Increased Gastric Cancer Risk
Two copies of the A allele are associated with a significantly higher risk of gastric cancer and acute graft-versus-host disease. This genetic profile is also linked to altered responses to specific immunosuppressive and pain medications.
What this genotype means: Approximately 3x higher risk of gastric cancer; Poorer response to TNF-alpha inhibitors.
Sample genotype (not yours): G/A
Moderately Increased Gastric Cancer Risk
A single copy of the A allele is linked to a moderately higher risk of developing gastric cancer and acute graft-versus-host disease. It may also influence how the body responds to certain anti-inflammatory and pain medications.
What this genotype means: Approximately 1.4x higher risk of gastric cancer; Poorer response to TNF-alpha inhibitors.
Gene function and biological role
Gene Function: Interleukin 17A encodes a pro-inflammatory cytokine that plays a central role in host defense against pathogens and the pathogenesis of various autoimmune and inflammatory diseases [1]. This cytokine is primarily produced by a specialized subset of T helper cells known as Th17 cells [2]. By binding to its receptors, it triggers the release of other inflammatory molecules, recruiting immune cells to sites of infection or injury [1]. However, persistent or excessive activity of this cytokine can lead to chronic tissue damage and has been implicated in the development of several types of cancer [2].
Variant Impact: Located in the promoter region of the IL17A gene, rs2275913 alters the transcription rate and subsequent expression levels of the interleukin 17A cytokine [2]. The change from a guanine to an adenine nucleotide at this position is functionally associated with increased promoter activity and higher cytokine production [2]. Elevated levels of this pro-inflammatory cytokine can drive chronic inflammatory states, which are known to promote cellular damage and tumor development [3]. Consequently, this genetic variation has been widely studied for its influence on susceptibility to inflammatory disorders, autoimmune conditions, and various cancers [3].
Key Insight: The A allele of this variant increases the production of the inflammatory cytokine IL-17A, which can promote tumor growth in the stomach.
Location: IL17A. Chromosome 6 · 6p12.2 · 52.2 Mb
Estimated prevalence by population
Global 53.0%; European 41.4%; African 81.8%; East Asian 28.6%; South Asian 37.9%; Americas 57.5%; Ashkenazi 50.0%; Finnish 27.9%; Middle Eastern 53.2%; Amish 46.3%.
Estimated GG genotype frequency.
Global 37.4%; European 45.9%; African 17.3%; East Asian 49.8%; South Asian 47.3%; Americas 36.7%; Ashkenazi 41.4%; Finnish 49.8%; Middle Eastern 39.5%; Amish 43.5%.
Estimated GA genotype frequency.
Global 9.7%; European 12.7%; African 0.9%; East Asian 21.7%; South Asian 14.8%; Americas 5.8%; Ashkenazi 8.6%; Finnish 22.3%; Middle Eastern 7.3%; Amish 10.2%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cancer & Oncology
Gastrointestinal Cancers
Gastric Cancer. Evidence: 4/10. Source: PMID 26535650. Typical Risk.
Pharmacogenomics
Immunosuppressant & Biologic Response
Graft-Versus-Host Disease. Evidence: 5/10. Typical Risk.
Cyclosporine Response. Evidence: 5/10. Source: PMID 30799725. Higher Rejection Risk.
Pain Medication Response
Pain Drug Sensitivity. Evidence: 5/10. Source: PMID 30106258. Typical Sensitivity.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
TNF-Alpha Response. Evidence: 5/10. Source: PMID 24776844. Typical Response.
Chronic Inflammatory Diseases
Ulcerative Colitis. Evidence: 3/10. Source: PMID 22955700. Typical Risk.
Showing effects for A/A genotype
Gastric Cancer. Evidence: 4/10. Source: PMID 26535650. ~3x Increased Risk.
Graft-Versus-Host Disease. Evidence: 5/10. Increased Risk.
Cyclosporine Response. Evidence: 5/10. Source: PMID 30799725. Typical Risk.
Pain Drug Sensitivity. Evidence: 5/10. Source: PMID 30106258. Lower Sensitivity.
TNF-Alpha Response. Evidence: 5/10. Source: PMID 24776844. Poorer Response.
Ulcerative Colitis. Evidence: 3/10. Source: PMID 22955700. Increased Risk.
Showing effects for G/A genotype
Gastric Cancer. Evidence: 4/10. Source: PMID 26535650. ~1.4x Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Guanine at both positions represents the baseline genetic profile for the majority of the global population. This profile is associated with typical, non-elevated susceptibility to gastric cancer and acute graft-versus-host disease [1]. In the context of medical treatments, clinical studies suggest that the G/G genotype may experience a higher likelihood of organ rejection when taking the immunosuppressant cyclosporine [2]. Conversely, this baseline profile is linked to a standard response to tumor necrosis factor inhibitors and typical sensitivity to opioid pain medications [3]. Maintaining a healthy lifestyle and avoiding chronic stomach inflammation remain key preventive strategies [1].
Typical baseline risk of gastric cancer; Increased risk of cyclosporine-related organ rejection.
Sample genotype: AA (Homozygous)
Possessing two copies of the A allele is associated with a significantly higher risk of gastric cancer, with some studies reporting up to a 3-fold increase in susceptibility [1]. This genotype is also linked to an elevated risk of acute graft-versus-host disease after unrelated bone marrow transplantation. Regarding medication responses, a poorer response to tumor necrosis factor inhibitors is often exhibited [2]. Furthermore, clinical studies suggest that opioid pain medications are typically less effective [3]. Proactive management of chronic stomach inflammation, such as Helicobacter pylori infection, is particularly important for individuals with this genetic profile [1].
Approximately 3x higher risk of gastric cancer; Poorer response to TNF-alpha inhibitors.
Sample genotype: GA (Heterozygous)
Inheriting one copy of the A allele is associated with a moderately elevated risk of gastric cancer, with studies reporting an approximate 1.4-fold increase in susceptibility [1]. This genetic variation is also linked to an increased risk of developing acute graft-versus-host disease following unrelated bone marrow transplantation. In terms of pharmacogenomics, a poorer response to tumor necrosis factor inhibitors used for inflammatory conditions has been observed [2]. Additionally, clinical observations indicate that opioid pain medications may be less effective [3]. Regular health screenings and discussing these genetic factors with a physician can help manage these potential risks [1].
Approximately 1.4x higher risk of gastric cancer; Poorer response to TNF-alpha inhibitors.
Variants with shared genetic architecture
rs3748067 · IL17A Gene · Chr 6 · Inflammatory Disease Risk
rs3819024 · IL17A Gene · Chr 6 · Inflammatory Disease Risk
rs8193036 · IL17A Gene · Chr 6 · Asthma and Inflammation Risk
Role of IL-17 gene polymorphisms in the susceptibility to gastric cancer.
Meta-analysis of associations between interleukin-17 gene polymorphisms and risk of gastric cancer.
Content updated August 2026.
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