What you carry at this position in your DNA and what research says about it.
Type 2 Diabetes Risk: 10/10 evidence, 71 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): T/T
Higher Risk of Type 2 Diabetes
Two copies of the T allele are associated with a significantly higher risk of developing type 2 diabetes. This genotype may also lead to higher fasting blood glucose and HbA1c levels.
What this genotype means: Significantly higher risk of type 2 diabetes; Elevated blood glucose and HbA1c levels; Better therapeutic response to sulfonylureas.
Sample genotype (not yours): C/C
Typical Risk of Type 2 Diabetes
Two copies of the C allele are associated with a typical risk of type 2 diabetes. This genotype is linked to optimal insulin secretion and normal blood sugar levels.
What this genotype means: Typical baseline risk of type 2 diabetes; Normal insulin secretion and blood sugar levels; Standard response to oral diabetes medications.
Sample genotype (not yours): T/C
Moderately Increased Risk of Type 2 Diabetes
One copy of the T allele is linked to a moderately increased risk of type 2 diabetes. This genetic setup also slightly elevates blood glucose and HbA1c levels.
What this genotype means: Moderately higher risk of type 2 diabetes; Slightly elevated blood glucose and HbA1c levels; Favorable response to sulfonylureas and metformin.
Gene function and biological role
Gene Function: The KCNJ11 gene encodes Kir6.2, a crucial subunit of the ATP-sensitive potassium channel found in pancreatic beta cells [1]. This channel plays a central role in regulating insulin secretion in response to blood glucose levels [1]. When glucose levels rise, ATP production increases, closing the channel and triggering insulin release [1]. Genetic variations in this gene can alter channel activity, directly affecting how much insulin is released [2]. Consequently, KCNJ11 is a major candidate gene for susceptibility to metabolic conditions like type 2 diabetes [2].
Variant Impact: The rs5219 variant, also known as E23K, is a missense mutation that changes the amino acid at position 23 from glutamate to lysine [1]. This molecular change makes the potassium channel slightly less sensitive to ATP, meaning it remains open longer than usual [1]. As a result, pancreatic beta cells release less insulin in response to glucose, leading to higher blood sugar levels [1]. This specific change is widely recognized as a risk factor for developing type 2 diabetes [2]. It also influences how patients respond to certain oral diabetes medications [3].
Key Insight: Although the T allele increases the risk of developing type 2 diabetes, individuals with this allele actually show a better therapeutic response to sulfonylurea medications.
Location: KCNJ11. Chromosome 11 · 11p15.1 · 17.4 Mb
Estimated prevalence by population
Global 10.1%; European 13.2%; African 0.4%; East Asian 12.5%; South Asian 14.0%; Americas 10.8%; Ashkenazi 12.6%; Finnish 21.9%; Middle Eastern 8.7%; Amish 26.7%.
Estimated TT genotype frequency.
Global 37.0%; European 46.2%; African 12.5%; East Asian 45.7%; South Asian 46.8%; Americas 44.1%; Ashkenazi 45.8%; Finnish 49.8%; Middle Eastern 41.6%; Amish 49.9%.
Estimated TC genotype frequency.
Global 53.0%; European 40.6%; African 87.1%; East Asian 41.7%; South Asian 39.2%; Americas 45.2%; Ashkenazi 41.7%; Finnish 28.3%; Middle Eastern 49.8%; Amish 23.4%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. ~1.26x to 2.5x Risk.
Blood Glucose. Evidence: 10/10. Source: PMID 39024449. Increased.
HbA1c. Evidence: 8/10. Source: PMID 39024449. Increased.
Heart Disease
Coronary Artery Disease. Evidence: 7/10. Source: PMID 41022758. Increased Risk.
Pharmacogenomics
Diabetes Medication Response
Sulfonylurea Response. Evidence: 6/10. Source: PMID 25115353. Stronger Response.
Showing effects for C/C genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. Typical Risk.
Blood Glucose. Evidence: 10/10. Source: PMID 39024449. Typical.
HbA1c. Evidence: 8/10. Source: PMID 39024449. Typical.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 41022758. Typical Risk.
Sulfonylurea Response. Evidence: 6/10. Source: PMID 25115353. Typical Response.
Showing effects for T/C genotype
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. ~1.1x to 1.3x Risk.
Blood Glucose. Evidence: 10/10. Source: PMID 39024449. Slightly Increased.
HbA1c. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 41022758. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Two copies of the T allele (the Lys23 variant) are linked to a roughly 1.26-fold to 2.5-fold increased risk of developing type 2 diabetes [1]. This genetic change reduces insulin secretion from pancreatic beta cells, causing blood sugar levels to rise more easily [2]. Individuals with this genotype also tend to have higher HbA1c levels, a key marker of long-term blood sugar control [3]. Furthermore, this variant is associated with an increased risk of coronary artery disease, particularly in those who already have diabetes [4]. On the positive side, if diabetes does develop, people with this genotype often show a significantly better response to sulfonylurea medications [5].
Significantly higher risk of type 2 diabetes; Elevated blood glucose and HbA1c levels; Better therapeutic response to sulfonylureas.
Sample genotype: CC (Homozygous)
Two copies of the C allele (the Glu23 variant) represent the baseline, protective genotype for metabolic health [1]. This genotype is associated with normal insulin secretion from pancreatic beta cells in response to glucose [2]. As a result, individuals typically maintain healthy blood sugar and HbA1c levels [3]. The risk of developing coronary artery disease is not elevated by this genetic marker [4]. While this genotype is highly favorable for avoiding diabetes, individuals who do develop the condition may show a more typical, rather than enhanced, response to sulfonylurea therapies [5]. Standard lifestyle recommendations for metabolic health still apply to maintain this protective baseline. Regular exercise and balanced nutrition remain essential for long-term well-being.
Typical baseline risk of type 2 diabetes; Normal insulin secretion and blood sugar levels; Standard response to oral diabetes medications.
Sample genotype: TC (Heterozygous)
One copy of the T allele combined with one copy of the C allele is associated with a moderate increase in type 2 diabetes risk, estimated at about 1.1-fold to 1.3-fold [1]. This heterozygous genotype leads to a partial reduction in insulin secretion compared to the protective genotype [2]. Consequently, individuals may experience slightly higher fasting glucose and HbA1c levels [3]. There is also a modest increase in the risk of developing coronary artery disease over time [4]. However, this genotype is linked to a more favorable response to oral diabetes medications like sulfonylureas and metformin [5]. Adopting healthy lifestyle habits can significantly offset this moderate genetic predisposition. Regular physical activity and a balanced diet are key components of a preventative wellness plan.
Moderately higher risk of type 2 diabetes; Slightly elevated blood glucose and HbA1c levels; Favorable response to sulfonylureas and metformin.
Variants with shared genetic architecture
rs5215 · KCNJ11 Gene · Chr 11 · Type 2 Diabetes Risk
rs10096633 · LPL Gene · Chr 8 · Triglycerides and Heart Health
rs10811661 · CDKN2B Gene · Chr 9 · Type 2 Diabetes Risk
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com