What you carry at this position in your DNA and what research says about it.
Inflammation and Aneurysm Risk: 10/10 evidence, 32 publications.
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Sample genotype (not yours): G/G
Typical Inflammation Levels and Lower Aneurysm Risk
Lower baseline levels of C-reactive protein characterize this genetic profile, which is linked to a reduced risk of inflammatory conditions. It also correlates with a highly favorable response to the lipid-lowering medication fenofibrate.
What this genotype means: Typical baseline C-reactive protein levels; Lower risk of abdominal aortic aneurysm; Better response to fenofibrate treatment.
Sample genotype (not yours): A/A
Higher Inflammation and Elevated Aneurysm Risk
Significantly higher baseline levels of C-reactive protein are associated with this genetic profile, raising the risk of cardiovascular and inflammatory conditions. It also correlates with a reduced anti-inflammatory response to fenofibrate.
What this genotype means: Elevated baseline C-reactive protein levels; Increased risk of abdominal aortic aneurysm; Poor response to fenofibrate treatment.
Sample genotype (not yours): G/A
Moderately Elevated Inflammation and Typical Aneurysm Risk
Slightly higher baseline levels of C-reactive protein are common with this intermediate genetic profile. This moderate elevation may subtly influence cardiovascular and inflammatory risks while maintaining a typical response to fenofibrate.
What this genotype means: Slightly elevated baseline C-reactive protein; Moderate response to fenofibrate treatment.
Gene function and biological role
Gene Function: The CRP gene encodes C-reactive protein, a key biomarker of systemic inflammation produced by the liver in response to inflammatory signals. Circulating levels of this protein rise during acute and chronic inflammatory states, serving as a clinical indicator of infection, tissue injury, and cardiovascular risk [1]. Genetic variations in the CRP promoter region directly influence how much of this protein is produced under baseline conditions [2]. Understanding these genetic baselines helps distinguish between chronic, genetically driven low-grade inflammation and acute inflammatory spikes.
Variant Impact: The rs3091244 variant is a triallelic single nucleotide polymorphism located in the promoter region of the CRP gene. This specific genetic change alters transcription factor binding, directly affecting the baseline expression and circulating levels of C-reactive protein [2]. The minor A allele is strongly linked to elevated baseline CRP levels, reflecting a heightened state of low-grade systemic inflammation [1]. This genetically driven elevation can influence long-term cardiovascular health. This card describes the two most common alleles, G and A. A third T allele, about 13% of copies worldwide and 6% in Europeans, is not covered here.
Key Insight: This genetic variant can cause baseline inflammation markers to appear elevated even in the complete absence of an active infection.
Location: CRP. Chromosome 1 · 1q23.2 · 159.7 Mb
Estimated prevalence by population
Global 49.3%; European 47.0%; African 50.3%; East Asian 88.1%; South Asian 56.9%; Americas 46.4%; Ashkenazi 48.3%; Finnish 41.7%; Middle Eastern 59.6%; Amish 41.6%.
Estimated GG genotype frequency.
Global 41.5%; European 43.1%; African 41.2%; East Asian 11.6%; South Asian 37.0%; Americas 43.4%; Ashkenazi 42.4%; Finnish 45.8%; Middle Eastern 35.2%; Amish 45.8%.
Estimated GA genotype frequency.
Global 9.2%; European 9.9%; African 8.5%; East Asian 0.4%; South Asian 6.0%; Americas 10.2%; Ashkenazi 9.3%; Finnish 12.6%; Middle Eastern 5.2%; Amish 12.6%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
C-Reactive Protein. Evidence: 10/10. Source: PMID 18439548. Typical Levels.
Cardiovascular & Metabolic
Heart Disease
Coronary Artery Disease. Evidence: 3/10. Source: PMID 16731635. Not established.
Vascular Health & Aneurysm
Aortic Aneurysm. Evidence: 3/10. Source: PMID 24135623. Lower Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Fenofibrate Response. Evidence: 5/10. Source: PMID 18285551. Stronger Response.
Organ Systems
Bone, Joint & Connective Tissue Health
Hand Osteoarthritis. Evidence: 3/10. Source: PMID 18055473. Not established.
Showing effects for A/A genotype
C-Reactive Protein. Evidence: 10/10. Source: PMID 18439548. Elevated Levels.
Aortic Aneurysm. Evidence: 3/10. Source: PMID 24135623. Increased Risk.
Fenofibrate Response. Evidence: 5/10. Source: PMID 18285551. Poor Response.
Showing effects for G/A genotype
C-Reactive Protein. Evidence: 10/10. Source: PMID 18439548. Slightly Elevated.
Aortic Aneurysm. Evidence: 3/10. Source: PMID 24135623. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
The presence of two common G alleles is associated with lower baseline levels of C-reactive protein, a key marker of systemic inflammation [1]. Because of these lower baseline levels, individuals with this genotype generally have a lower risk of developing inflammatory and cardiovascular conditions, such as abdominal aortic aneurysms [2]. Additionally, research shows that people with the G/G genotype experience a more significant reduction in CRP levels when treated with the cholesterol-lowering drug fenofibrate [3]. This suggests a better overall anti-inflammatory response to certain cardiovascular therapies. Maintaining a healthy lifestyle further supports this naturally lower inflammatory profile.
Typical baseline C-reactive protein levels; Lower risk of abdominal aortic aneurysm; Better response to fenofibrate treatment.
Sample genotype: AA (Homozygous)
Two copies of the minor A allele tend to produce the highest baseline levels of C-reactive protein, indicating a genetic predisposition to low-grade systemic inflammation [1]. This chronic inflammatory state is associated with a significantly higher risk of developing abdominal aortic aneurysms [2]. Furthermore, studies indicate that individuals carrying the A/A genotype show almost no reduction in CRP levels when taking the lipid-lowering medication fenofibrate, suggesting a poor therapeutic response [3]. Managing systemic inflammation through anti-inflammatory dietary choices and regular physical activity is particularly beneficial for this genetic profile.
Elevated baseline C-reactive protein levels; Increased risk of abdominal aortic aneurysm; Poor response to fenofibrate treatment.
Sample genotype: GA (Heterozygous)
A single copy of the minor A allele leads to intermediate baseline levels of C-reactive protein, placing individuals between the lower-risk G/G genotype and the higher-risk A/A genotype [1]. This moderate elevation in systemic inflammation can slightly influence the long-term risk of developing conditions like abdominal aortic aneurysms [2]. However, the presence of one G allele still allows for a relatively favorable anti-inflammatory response to fenofibrate therapy compared to those with two copies of the risk allele [3]. Routine monitoring of cardiovascular health and managing lifestyle factors like diet and exercise can help keep overall inflammation in check.
Slightly elevated baseline C-reactive protein; Moderate response to fenofibrate treatment.
Variants with shared genetic architecture
rs7553007 · CRP Gene · Chr 1 · C-Reactive Protein Levels
rs1800947 · CRP Gene · Chr 1 · C-Reactive Protein Levels
rs1205 · CRP Gene · Chr 1 · C-Reactive Protein Levels
C-reactive protein polymorphism rs3091244 is associated with abdominal aortic aneurysm.
Content updated August 2026.
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