What you carry at this position in your DNA and what research says about it.
Stroke and Blood Pressure Risk: 5/10 evidence, 73 publications.
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Sample genotype (not yours): C/C
Typical Stroke and Blood Pressure Risk
Standard enzyme function maintains typical vitamin K clearance and blood pressure regulation. Standard doses of blood-thinning medications are highly effective.
What this genotype means: Typical stroke risk; Standard blood pressure regulation; Standard response to blood thinners.
Sample genotype (not yours): C/T
Slightly Elevated Stroke and Blood Pressure Risk
Reduced enzyme activity leads to slower vitamin K clearance and slightly higher blood pressure. Reduced response to blood-thinning medications.
What this genotype means: Slightly increased stroke risk; Slightly elevated blood pressure risk; Reduced warfarin response.
Sample genotype (not yours): T/T
Elevated Stroke and Blood Pressure Risk
Significantly reduced enzyme activity leads to slower vitamin K clearance and elevated blood pressure. Substantially reduced response to blood thinners.
What this genotype means: Increased stroke risk; Elevated blood pressure risk; Significantly reduced warfarin response.
Gene function and biological role
Gene Function: The CYP4F2 gene encodes a member of the cytochrome P450 superfamily of enzymes that plays a critical role in lipid metabolism [1]. This enzyme acts as a primary catalyst in the breakdown of fat-soluble vitamins, specifically functioning as a vitamin K1 oxidase [2]. By regulating the degradation of vitamin K, it directly influences the availability of active clotting factors in the body [2]. Additionally, the enzyme metabolizes arachidonic acid into 20-hydroxyeicosatetraenoic acid (20-HETE), a key signaling molecule involved in regulating blood pressure and renal function [3]. It also participates in the metabolic clearance of tocopherols, thereby modulating circulating vitamin E levels [4].
Variant Impact: The rs2108622 variant is a missense mutation in the CYP4F2 gene that results in a valine-to-methionine substitution at position 433 of the protein [5]. This structural change significantly reduces the enzyme's ability to oxidize and degrade vitamin K1 [2]. Consequently, the altered enzyme leads to an accumulation of vitamin K and vitamin E in the body [4]. Because vitamin K is a crucial cofactor for blood clotting, this reduction in clearance directly alters how the body responds to anticoagulant medications [6]. The variant also disrupts the balance of bioactive lipid mediators, which has downstream effects on vascular tone and cardiovascular health [3].
Key Insight: This variant acts as a genetic dial for vitamin K, where lower enzyme activity actually increases circulating vitamin K and vitamin E levels, directly altering blood-thinning medication requirements.
Location: CYP4F2. Chromosome 19 · 19p13.12 · 15.9 Mb
Estimated prevalence by population
Global 60.1%; European 50.9%; African 81.2%; East Asian 56.9%; South Asian 35.9%; Americas 55.1%; Ashkenazi 42.6%; Finnish 64.2%; Middle Eastern 37.1%; Amish 63.6%.
Estimated CC genotype frequency.
Global 33.8%; European 40.9%; African 17.8%; East Asian 37.1%; South Asian 48.0%; Americas 38.3%; Ashkenazi 45.3%; Finnish 31.9%; Middle Eastern 47.6%; Amish 32.3%.
Estimated CT genotype frequency.
Global 6.0%; European 8.2%; African 1.0%; East Asian 6.1%; South Asian 16.1%; Americas 6.7%; Ashkenazi 12.1%; Finnish 4.0%; Middle Eastern 15.3%; Amish 4.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Stroke
Stroke. Evidence: 5/10. Source: PMID 29273767. Typical Risk.
Hypertension
Blood Pressure. Evidence: 3/10. Source: PMID 21625857. Typical.
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Anticoagulant Response. Evidence: 9/10. Source: PMID 19300499. Typical Response.
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin K Levels. Evidence: 6/10. Source: PMID 25411281. Typical Levels.
Vitamin E Levels. Evidence: 6/10. Source: PMID 21729881. Typical Levels.
Showing effects for C/T genotype
Stroke. Evidence: 5/10. Source: PMID 29273767. Increased Risk.
Blood Pressure. Evidence: 3/10. Source: PMID 21625857. Slightly Elevated.
Anticoagulant Response. Evidence: 9/10. Source: PMID 19300499. Higher Tolerance.
Vitamin K Levels. Evidence: 6/10. Source: PMID 25411281. Slightly Higher.
Vitamin E Levels. Evidence: 6/10. Source: PMID 21729881. Slightly Higher.
Showing effects for T/T genotype
Stroke. Evidence: 5/10. Source: PMID 29273767. Higher Risk.
Blood Pressure. Evidence: 3/10. Source: PMID 21625857. Elevated.
Vitamin K Levels. Evidence: 6/10. Source: PMID 25411281. Higher Levels.
Vitamin E Levels. Evidence: 6/10. Source: PMID 21729881. Higher Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Normal enzyme activity in the liver ensures typical processing of fat-soluble vitamins and fatty acids [1]. Because vitamin K is degraded at a standard rate, baseline levels of this essential clotting cofactor remain within the typical range [2]. Consequently, standard doses of blood-thinning medications like warfarin are highly effective and do not require genetic adjustments [3]. Maintaining typical enzyme function also supports a healthy balance of lipid signaling molecules like 20-HETE, which helps regulate blood pressure [4]. Studies show that this baseline state is associated with a lower risk of developing ischemic stroke compared to carriers of the variant allele [5]. Overall cardiovascular health and vascular tone are typically well-regulated under this genetic profile [6].
Typical stroke risk; Standard blood pressure regulation; Standard response to blood thinners.
Sample genotype: CT (Heterozygous)
A single copy of the decreased-function variant reduces the liver's ability to break down vitamin K1 [1]. This slower clearance leads to slightly higher circulating levels of vitamin K and vitamin E in the blood [2]. When taking vitamin K antagonists such as warfarin or acenocoumarol, the blood-thinning effect is typically weaker [3]. The reduction in enzyme activity also alters the production of 20-HETE, a lipid mediator that regulates blood vessel constriction [4]. This biochemical shift is linked to a slightly elevated risk of developing high blood pressure [5]. Furthermore, clinical studies have observed an increased susceptibility to ischemic stroke in individuals with this intermediate profile [6].
Slightly increased stroke risk; Slightly elevated blood pressure risk; Reduced warfarin response.
Sample genotype: TT (Homozygous)
Two copies of the decreased-function variant severely limit the enzyme's capacity to degrade vitamin K1 [1]. Slower metabolism results in significantly elevated baseline levels of both vitamin K and vitamin E [2]. Because of the abundance of active vitamin K, blood thinners like warfarin are often substantially less effective [3]. The marked reduction in enzyme function also disrupts the synthesis of 20-HETE, impairing the body's natural regulation of vascular tone [4]. This disruption is strongly associated with an increased risk of essential hypertension [5]. Clinical evidence indicates a significantly higher risk of ischemic stroke, particularly in males and those with other cardiovascular risk factors [6].
Increased stroke risk; Elevated blood pressure risk; Significantly reduced warfarin response.
Variants with shared genetic architecture
rs2359612 · VKORC1 Gene · Chr 16 · Cardiovascular Risk
rs7294 · VKORC1 Gene · Chr 16 · Vitamin K and Bone Health
rs8050894 · VKORC1 Gene · Chr 16 · Warfarin Sensitivity
Systematic genetic and genomic analysis of cytochrome P450 enzyme activities in human liver.
CYP4F2 genetic variant alters required warfarin dose.
Association of 1347 G/A cytochrome P450 4F2 (CYP4F2) gene variant with hypertension and stroke.
A genome-wide association study of acenocoumarol maintenance dosage.
Content updated August 2026.
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