What you carry at this position in your DNA and what research says about it.
Warfarin Sensitivity: 8/10 evidence, 21 publications.
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Sample genotype (not yours): A/A
Typical Warfarin Sensitivity
A typical response to warfarin is expected.
What this genotype means: Typical warfarin response; Typical bleeding risk on therapy; Typical bone mineral density.
Sample genotype (not yours): A/C
Increased Warfarin Sensitivity
This VKORC1 variant reduces the amount of vitamin K recycling enzyme available, which is the target warfarin acts on. VKORC1 genotype is one of the inputs prescribing guidelines use for warfarin; any decision about a medicine is your prescriber's.
What this genotype means: Greater warfarin sensitivity; Increased risk of over-anticoagulation; Slightly lower bone mineral density.
Sample genotype (not yours): C/C
High Warfarin Sensitivity
Substantially greater sensitivity to warfarin, with a risk of severe bleeding.
What this genotype means: Significantly greater warfarin sensitivity; High risk of bleeding on standard doses; Decreased bone mineral density.
Gene function and biological role
Gene Function: The VKORC1 gene encodes the vitamin K epoxide reductase complex subunit 1 enzyme, which plays a critical role in the vitamin K cycle [1]. This enzyme converts vitamin K epoxide back into its active, reduced form, which is essential for the gamma-carboxylation of clotting factors [1]. Without sufficient activity of this enzyme, the body cannot properly activate key proteins involved in blood coagulation [2]. Because of this central role, the gene is the primary therapeutic target for the widely prescribed oral anticoagulant medication warfarin [3]. Genetic variations within this gene are major determinants of how sensitive a person is to warfarin therapy [3].
Variant Impact: The rs2884737 variant is an intronic change located within the VKORC1 gene that influences the expression and availability of the vitamin K reductase enzyme [2]. This genetic alteration is highly linked to other functional variants in the gene that dictate how the body processes vitamin K and responds to anticoagulant drugs [2]. Carrying the variant C allele reduces the overall expression of the enzyme, making the clotting process more sensitive to inhibition [4].
Key Insight: This variant is a primary genetic factor determining warfarin dosage, and carrying the C allele can significantly increase bleeding risk if standard doses are prescribed.
Location: VKORC1. Chromosome 16 · 16p11.2 · 31.1 Mb
Estimated prevalence by population
Global 68.3%; European 54.8%; African 91.2%; East Asian 99.7%; South Asian 83.3%; Americas 64.6%; Ashkenazi 44.3%; Finnish 60.3%; Middle Eastern 32.3%; Amish 56.2%.
Estimated AA genotype frequency.
Global 27.4%; European 38.5%; African 8.6%; East Asian 0.3%; South Asian 16.0%; Americas 31.6%; Ashkenazi 44.5%; Finnish 34.7%; Middle Eastern 49.1%; Amish 37.5%.
Estimated AC genotype frequency.
Global 4.3%; European 6.7%; African 0.2%; East Asian < 0.1%; South Asian 0.8%; Americas 3.9%; Ashkenazi 11.2%; Finnish 5.0%; Middle Eastern 18.6%; Amish 6.3%.
Estimated CC genotype frequency.
Showing effects for A/A genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Warfarin Sensitivity. Evidence: 8/10. Source: PMID 16611750. Typical Response.
Organ Systems
Bone, Joint & Connective Tissue Health
Bone Mineral Density. Evidence: 3/10. Source: PMID 21179439. Typical Density.
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin K Status. Evidence: 3/10. Source: PMID 19436136. Typical Status.
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 6/10. Source: PMID 41044249. Higher Ratio.
Showing effects for A/C genotype
Warfarin Sensitivity. Evidence: 8/10. Source: PMID 16611750. Higher Sensitivity.
Bone Mineral Density. Evidence: 3/10. Source: PMID 21179439. Slightly Decreased.
Vitamin K Status. Evidence: 3/10. Source: PMID 19436136. Altered Status.
HDL Cholesterol. Evidence: 6/10. Source: PMID 41044249. Typical Ratio.
Showing effects for C/C genotype
Warfarin Sensitivity. Evidence: 8/10. Source: PMID 16611750. Much Higher Sensitivity.
Bone Mineral Density. Evidence: 3/10. Source: PMID 21179439. Decreased.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Standard levels of the vitamin K epoxide reductase enzyme are typically maintained by those with the common A/A genotype [1]. Because enzyme activity remains at baseline, a typical response to warfarin is expected [1]. Clinical studies show that people with this genotype are less sensitive to warfarin compared to those carrying the C allele [2]. Initiating therapy with standard dosing algorithms is less likely to cause unexpected over-anticoagulation or bleeding complications [2]. The target international normalized ratio may sometimes be slightly harder to reach than in the population average [3]. Beyond medication response, this genotype is linked to typical bone mineral density and standard vitamin K status [4]. Most global populations carry this common genetic profile, making it the standard reference group for pharmacogenomic dosing guidelines [3]. Regular dietary intake of vitamin K-rich foods generally interacts normally with this baseline enzyme activity [4].
Typical warfarin response; Typical bleeding risk on therapy; Typical bone mineral density.
Sample genotype: AC (Heterozygous)
Moderate sensitivity to the blood-thinning medication warfarin is commonly observed in the presence of a single C allele [1]. This increased sensitivity occurs because the C allele is linked to lower expression of the vitamin K epoxide reductase enzyme, making clotting factors easier to suppress [2]. Standard doses of the medication may lead to a higher-than-expected international normalized ratio, increasing the risk of minor bleeding events [3]. Close monitoring during the initiation phase of therapy is highly recommended by expert panels to safely establish the correct dosage [4]. Additionally, some research suggests a potential association with subtle variations in bone mineral density [5]. Understanding this genetic trait helps clinicians tailor anticoagulant therapy more precisely from the very beginning of treatment [4]. Dietary vitamin K intake remains an important factor to balance alongside any prescribed medication adjustments [2].
Greater warfarin sensitivity; Increased risk of over-anticoagulation; Slightly lower bone mineral density.
Sample genotype: CC (Homozygous)
Pronounced reduction in the expression of the vitamin K epoxide reductase enzyme occurs when two copies of the C allele are present [1]. This biological change makes the blood clotting cascade highly sensitive to the inhibitory effects of oral anticoagulants like warfarin [1]. Clinical data indicate that individuals with this genotype are substantially more sensitive to warfarin than those with the common genotype [2]. Administering standard doses of warfarin to someone with this genetic profile carries a high risk of over-anticoagulation, which can lead to severe bleeding complications [3]. Because of this high sensitivity, pharmacogenomic dosing algorithms heavily weigh this genetic marker to prevent adverse drug events [4]. Research also indicates that this genetic variation may be associated with decreased bone mineral density in certain populations [5]. Regular bone density assessments and adequate calcium intake may be beneficial considerations for long-term skeletal health [5]. Healthcare providers routinely utilize these genetic insights to bypass the traditional trial-and-error approach to anticoagulation [4].
Significantly greater warfarin sensitivity; High risk of bleeding on standard doses; Decreased bone mineral density.
Variants with shared genetic architecture
rs2359612 · VKORC1 Gene · Chr 16 · Cardiovascular Risk
rs61742245 · VKORC1 Gene · Chr 16 · Warfarin Resistance
rs7294 · VKORC1 Gene · Chr 16 · Vitamin K and Bone Health
Genetic determinants of response to warfarin during initial anticoagulation.
Content updated August 2026.
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