What you carry at this position in your DNA and what research says about it.
C-Reactive Protein Levels: 8/10 evidence, 51 publications.
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Sample genotype (not yours): C/C
Typical Lupus Risk and Higher Baseline Inflammation
This genotype is associated with typical baseline risks for autoimmune conditions but slightly higher levels of C-reactive protein and LDL cholesterol.
What this genotype means: Typical risk of autoimmune lupus; Slightly higher baseline C-reactive protein; Typical response to NSAIDs and warfarin.
Sample genotype (not yours): C/T
Increased Lupus Risk and Altered Drug Sensitivity
Carrying one copy of the T allele is linked to lower C-reactive protein levels, an increased risk of lupus, and altered responses to certain medications.
What this genotype means: Increased risk of systemic lupus erythematosus; Slightly lower baseline C-reactive protein; Elevated cardiovascular risk with NSAID use.
Sample genotype (not yours): T/T
Highest Lupus Risk and Lower Baseline Inflammation
Two copies of the T allele result in significantly lower C-reactive protein levels, which increases lupus susceptibility and alters drug safety profiles.
What this genotype means: Highest genetic risk of systemic lupus erythematosus; Significantly lower baseline C-reactive protein; Increased bleeding risk on warfarin.
Gene function and biological role
Gene Function: The CRP gene encodes C-reactive protein, a key biomarker of systemic inflammation synthesized by the liver in response to tissue injury or infection. Circulating levels of this protein rise rapidly during acute inflammatory states and serve as a clinical indicator for cardiovascular risk and chronic inflammatory conditions [1]. Beyond acting as a simple marker, C-reactive protein plays an active role in the immune system by binding to damaged cells and pathogens to facilitate their clearance. However, genetically determined baseline levels of this protein vary widely among individuals, influencing susceptibility to autoimmune disorders and cardiovascular events [2].
Variant Impact: The rs1205 variant is a single nucleotide polymorphism located in the 3 prime untranslated region of the CRP gene that directly alters gene expression. The minor T allele is strongly associated with significantly lower baseline levels of circulating C-reactive protein [1]. While lower inflammation markers are generally considered favorable, abnormally low C-reactive protein can impair the clearance of dying cells, increasing the risk of autoimmune diseases like lupus. Additionally, this genetic variation alters how the body responds to certain medications, including nonsteroidal anti-inflammatory drugs and blood thinners [3].
Key Insight: While high C-reactive protein is a well-known marker of chronic inflammation, genetically low levels of this protein can actually increase the risk of developing lupus by hindering the body's ability to clear cellular debris.
Location: CRP. Chromosome 1 · 1q23.2 · 159.7 Mb
Estimated prevalence by population
Global 48.3%; European 44.4%; African 64.7%; East Asian 17.6%; South Asian 48.2%; Americas 39.4%; Ashkenazi 40.9%; Finnish 39.6%; Middle Eastern 46.4%; Amish 60.4%.
Estimated CC genotype frequency.
Global 41.3%; European 44.5%; African 31.5%; East Asian 48.7%; South Asian 42.4%; Americas 46.8%; Ashkenazi 46.1%; Finnish 46.7%; Middle Eastern 43.4%; Amish 34.7%.
Estimated CT genotype frequency.
Global 10.3%; European 11.1%; African 3.8%; East Asian 33.6%; South Asian 9.3%; Americas 13.9%; Ashkenazi 13.0%; Finnish 13.8%; Middle Eastern 10.1%; Amish 5.0%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
C-Reactive Protein. Evidence: 8/10. Source: PMID 33296257. Typical Levels.
Autoimmune Diseases
Lupus. Evidence: 3/10. Source: PMID 29556849. Typical Risk.
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 8/10. Source: PMID 36376304. Slightly Higher.
Pharmacogenomics
Adverse Drug Reactions
NSAID Heart Effects. Evidence: 5/10. Source: PMID 20538124. Typical Risk.
Anticoagulant & Blood Thinner Response
Warfarin Bleeding Risk. Evidence: 5/10. Source: PMID 24602049. Typical Risk.
Showing effects for C/T genotype
C-Reactive Protein. Evidence: 8/10. Source: PMID 33296257. ~20% Lower Levels.
Lupus. Evidence: 3/10. Source: PMID 29556849. Increased Risk.
LDL Cholesterol. Evidence: 8/10. Source: PMID 36376304. Typical.
NSAID Heart Effects. Evidence: 5/10. Source: PMID 20538124. Increased Risk.
Warfarin Bleeding Risk. Evidence: 5/10. Source: PMID 24602049. Increased Risk.
Showing effects for T/T genotype
C-Reactive Protein. Evidence: 8/10. Source: PMID 33296257. ~40% Lower Levels.
Lupus. Evidence: 3/10. Source: PMID 29556849. Higher Risk.
LDL Cholesterol. Evidence: 8/10. Source: PMID 36376304. Slightly Lower.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Individuals with this genotype tend to have higher baseline levels of circulating C-reactive protein compared to carriers of the T allele [1]. While higher C-reactive protein is a marker of low-grade chronic inflammation, it also supports the immune system's ability to clear cellular waste, resulting in a typical baseline risk for systemic lupus erythematosus. This genotype is also linked to slightly higher LDL cholesterol levels [2]. Additionally, those with this genotype show a typical cardiovascular response to nonsteroidal anti-inflammatory drugs and standard bleeding risks when taking warfarin [3].
Typical risk of autoimmune lupus; Slightly higher baseline C-reactive protein; Typical response to NSAIDs and warfarin.
Sample genotype: CT (Heterozygous)
Carrying a single copy of the T allele is associated with an approximate twenty percent reduction in baseline C-reactive protein levels [1]. Although lower systemic inflammation is generally beneficial, reduced C-reactive protein can hinder the clearance of apoptotic cells, which is linked to an increased susceptibility to systemic lupus erythematosus. This genotype is also associated with a slightly lower level of LDL cholesterol [2]. Furthermore, clinical studies suggest that carriers of this variant may experience an increased likelihood of acute coronary syndrome when using nonsteroidal anti-inflammatory drugs [3]. There is also an elevated risk of bleeding complications during warfarin therapy [4].
Increased risk of systemic lupus erythematosus; Slightly lower baseline C-reactive protein; Elevated cardiovascular risk with NSAID use.
Sample genotype: TT (Homozygous)
Having two copies of the T allele is associated with an approximate forty percent reduction in baseline C-reactive protein levels [1]. This substantial reduction in C-reactive protein can impair the body's natural process of clearing damaged cells, significantly increasing the risk of developing systemic lupus erythematosus. On the other hand, this genotype is linked to lower LDL cholesterol levels [2]. When taking medications, individuals with this genotype have an increased likelihood of experiencing acute coronary syndrome while on nonsteroidal anti-inflammatory drugs [3]. They also face a higher risk of bleeding complications when prescribed the blood thinner warfarin [4].
Highest genetic risk of systemic lupus erythematosus; Significantly lower baseline C-reactive protein; Increased bleeding risk on warfarin.
Variants with shared genetic architecture
rs3091244 · CRP Gene · Chr 1 · Inflammation and Aneurysm Risk
rs7553007 · CRP Gene · Chr 1 · C-Reactive Protein Levels
rs1800947 · CRP Gene · Chr 1 · C-Reactive Protein Levels
Genetic polymorphisms and the cardiovascular risk of non-steroidal anti-inflammatory drugs.
Pleiotropic genetic architecture and novel loci for C-reactive protein levels.
Content updated August 2026.
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