What you carry at this position in your DNA and what research says about it.
Cardiac QT Interval: 10/10 evidence, 15 publications.
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Sample genotype (not yours): T/T
Shorter QT Interval and Lower Arrhythmia Risk
Two copies of the protective T allele are associated with a shorter cardiac electrical reset time. This genotype provides a natural buffer against rhythm disturbances.
What this genotype means: Shorter cardiac QT interval; Reduced risk of cardiac arrhythmias; Faster electrical recovery of heart cells.
Sample genotype (not yours): C/C
Typical QT Interval and Standard Arrhythmia Risk
This common genotype is associated with typical cardiac electrical reset times. It does not carry the protective benefits of the rare T allele.
What this genotype means: Typical cardiac QT interval; Standard baseline risk for cardiac events; Typical potassium channel expression.
Sample genotype (not yours): T/C
One copy of the protective T allele is associated with a shorter cardiac electrical reset time. This genotype helps shield the heart from rhythm irregularities.
What this genotype means: Shorter cardiac QT interval; Reduced risk of cardiac arrhythmias; Enhanced electrical stability under stress.
Gene function and biological role
Gene Function: The KCNQ1 gene encodes the pore-forming subunit of a critical voltage-gated potassium channel in the heart. This channel generates the slow delayed rectifier potassium current, which is essential for repolarizing cardiac cells after each heartbeat [1]. Proper functioning of this channel ensures that the heart's electrical system resets correctly between beats. Mutations or variations in KCNQ1 can alter this electrical reset time, directly influencing the QT interval on an electrocardiogram [2].
Variant Impact: The rs2074238 variant is an intronic genetic change located within the KCNQ1 gene. Because it is located in a non-coding region, it does not directly alter the amino acid sequence of the potassium channel protein. Instead, research suggests this variant acts as a regulatory modifier that influences KCNQ1 gene expression in cardiac tissue [1]. By modulating expression, it affects the speed of ventricular repolarization and alters the duration of the heart's electrical cycle [3].
Key Insight: The rare T allele of this variant acts as a natural protective modifier that shortens the heart's electrical reset time and significantly lowers the risk of cardiac events.
Location: KCNQ1. Chromosome 11 · 11p15.5 · 2.5 Mb
Estimated prevalence by population
Global 0.4%; European 0.6%; African < 0.1%; East Asian 0.1%; South Asian 0.1%; Americas 0.2%; Ashkenazi 1.3%; Finnish 1.0%; Middle Eastern 0.3%; Amish < 0.1%.
Estimated TT genotype frequency.
Global 10.7%; European 14.8%; African 3.1%; East Asian 4.8%; South Asian 7.0%; Americas 9.4%; Ashkenazi 20.3%; Finnish 18.3%; Middle Eastern 10.3%; Amish 3.7%.
Estimated TC genotype frequency.
Global 88.8%; European 84.5%; African 96.9%; East Asian 95.2%; South Asian 92.9%; Americas 90.4%; Ashkenazi 78.4%; Finnish 80.7%; Middle Eastern 89.4%; Amish 96.3%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Heart Rhythm & Conduction
QT Interval. Evidence: 10/10. Source: PMID 19305408. Shorter QT Interval.
Cardiac Arrhythmia. Evidence: 3/10. Source: PMID 23856471. Reduced Risk.
JT Interval. Evidence: 8/10. Source: PMID 29874175. Shorter JT Interval.
T Wave Morphology. Evidence: 6/10. Source: PMID 31607149. Altered Shape.
Showing effects for C/C genotype
QT Interval. Evidence: 10/10. Source: PMID 19305408. Typical QT Interval.
Cardiac Arrhythmia. Evidence: 3/10. Source: PMID 23856471. Typical Risk.
JT Interval. Evidence: 8/10. Source: PMID 29874175. Typical JT Interval.
T Wave Morphology. Evidence: 6/10. Source: PMID 31607149. Typical Shape.
Showing effects for T/C genotype
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Carrying two copies of the minor T allele is associated with a significantly shorter QT interval on an electrocardiogram [1]. This shorter interval indicates that the heart muscle cells repolarize and reset their electrical state more rapidly after each contraction [2]. Clinical studies have identified this specific genotype as a powerful protective modifier against cardiac events, particularly in individuals who carry mutations predisposing them to Long QT Syndrome [1]. By accelerating the electrical recovery phase, this variant helps maintain a stable heart rhythm and reduces the likelihood of dangerous arrhythmias [1]. The protective effect is highly relevant for overall cardiovascular health and electrical stability.
Shorter cardiac QT interval; Reduced risk of cardiac arrhythmias; Faster electrical recovery of heart cells.
Sample genotype: CC (Homozygous)
Having two copies of the common C allele is the most frequent genetic profile globally, occurring in over ninety percent of most populations. This genotype is associated with typical QT interval durations and standard baseline risks for cardiac arrhythmias [1]. Unlike carriers of the rare T allele, individuals with this genotype do not benefit from the natural protective shortening of the electrical recovery phase [2]. While it does not represent an elevated risk compared to the general population, it lacks the genetic shield that helps mitigate rhythm disturbances under physiological stress or when taking certain medications [2]. Standard cardiovascular health guidelines and routine monitoring apply.
Typical cardiac QT interval; Standard baseline risk for cardiac events; Typical potassium channel expression.
Sample genotype: TC (Heterozygous)
Carrying one copy of the protective T allele is linked to a shorter QT interval compared to the common genotype [1]. This reduction in the QT interval reflects a more efficient electrical recovery process in the ventricles of the heart [2]. In clinical cohorts, carriers of this heterozygous genotype demonstrated a significantly lower risk of experiencing cardiac events, such as syncope or arrhythmias, even when other predisposing genetic risk factors were present [1]. The presence of the T allele appears to optimize the expression of the KCNQ1 potassium channel, thereby stabilizing the cardiac action potential [1]. This genetic buffer contributes to overall electrical resilience in the heart.
Shorter cardiac QT interval; Reduced risk of cardiac arrhythmias; Enhanced electrical stability under stress.
Variants with shared genetic architecture
rs2237895 · KCNQ1 Gene · Chr 11 · Type 2 Diabetes Risk
rs2237897 · KCNQ1 Gene · Chr 11 · Type 2 Diabetes Risk
rs2237892 · KCNQ1 Gene · Chr 11 · Type 2 Diabetes Risk
Common variants at ten loci influence QT interval duration in the QTGEN Study.
Content updated August 2026.
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