What you carry at this position in your DNA and what research says about it.
Chemotherapy Side Effects: 9/10 evidence, 13 publications.
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Sample genotype (not yours): A/A
Typical Chemotherapy Toxicity Risk and Optimal Carnitine Transport
Standard transporter function maintains healthy carnitine levels and typical red blood cell stability. There is no elevated risk of toxicity from specific chemotherapy drugs.
What this genotype means: Typical chemotherapy side effect risk; Optimal red blood cell stability.
Sample genotype (not yours): A/G
Moderately Increased Chemotherapy Toxicity Risk
A single copy of the variant allele slightly reduces transporter efficiency, which may influence drug processing. There is a moderately higher risk of side effects from certain chemotherapy medications.
What this genotype means: Moderately increased chemotherapy toxicity risk; Intermediate carnitine transport levels.
Sample genotype (not yours): G/G
Higher Chemotherapy Toxicity Risk and Reduced Carnitine Transport
Two copies of the variant significantly lower transporter efficiency, increasing the risk of chemotherapy side effects. Red blood cells may also show reduced stability and lower carnitine levels.
What this genotype means: Higher risk of chemotherapy side effects; Reduced red blood cell stability under stress.
Gene function and biological role
Gene Function: The SLC22A16 gene encodes a specialized transport protein known as organic cation transporter 6 or carnitine transporter 2. This protein is highly active in hematopoietic cells, where it regulates the cellular uptake of essential nutrients like L-carnitine [1]. It also plays a key role in transporting certain chemotherapy drugs into cells [2]. Proper functioning of this transporter is vital for maintaining cellular energy metabolism and protecting red blood cells from oxidative stress [1]. Variations in this gene can significantly alter how the body processes both dietary compounds and medical therapies [2].
Variant Impact: The rs12210538 variant is a missense mutation in the SLC22A16 gene that changes the amino acid at position 409 from methionine to threonine. This structural alteration directly impacts the transporter's ability to move L-carnitine and other organic cations across cell membranes [1]. Research indicates that the G allele reduces the transporter's efficiency, leading to lower levels of circulating acylcarnitines [3]. Conversely, this same genetic change alters cellular sensitivity to specific chemotherapy medications [2]. Understanding this variant helps clarify individual differences in metabolism and drug tolerance [2].
Key Insight: This variant affects both how your body transports energy-producing carnitines and how it processes common chemotherapy drugs.
Location: SLC22A16. Chromosome 6 · 6q21 · 110.4 Mb
Estimated prevalence by population
Global 71.8%; European 58.3%; African 91.9%; East Asian 99.7%; South Asian 80.0%; Americas 70.7%; Ashkenazi 53.7%; Finnish 72.1%; Middle Eastern 59.6%; Amish 47.1%.
Estimated AA genotype frequency.
Global 25.0%; European 36.1%; African 7.9%; East Asian 0.3%; South Asian 18.8%; Americas 26.8%; Ashkenazi 39.2%; Finnish 25.6%; Middle Eastern 35.2%; Amish 43.1%.
Estimated AG genotype frequency.
Global 3.3%; European 5.6%; African 0.2%; East Asian < 0.1%; South Asian 1.1%; Americas 2.5%; Ashkenazi 7.1%; Finnish 2.3%; Middle Eastern 5.2%; Amish 9.8%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Pharmacogenomics
Chemotherapy Response
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 20179710. Typical Risk.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Red Blood Cell Stability. Evidence: 9/10. Source: PMID 27863252. Optimal Stability.
Diabetes & Glycemic Traits
Blood Glucose. Evidence: 8/10. Source: PMID 39280063. Slightly Higher HbA1c.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Acylcarnitine Levels. Evidence: 8/10. Source: PMID 31882771. Higher Levels.
Ergothioneine Levels. Evidence: 9/10. Source: PMID 35050183. Lower Levels.
Showing effects for A/G genotype
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 20179710. Increased Risk.
Red Blood Cell Stability. Evidence: 9/10. Source: PMID 27863252. Moderate Stability.
Blood Glucose. Evidence: 8/10. Source: PMID 39280063. Typical HbA1c.
Acylcarnitine Levels. Evidence: 8/10. Source: PMID 31882771. Typical Levels.
Ergothioneine Levels. Evidence: 9/10. Source: PMID 35050183. Typical Levels.
Showing effects for G/G genotype
Red Blood Cell Stability. Evidence: 9/10. Source: PMID 27863252. Reduced Stability.
Blood Glucose. Evidence: 8/10. Source: PMID 39280063. Slightly Lower HbA1c.
Acylcarnitine Levels. Evidence: 8/10. Source: PMID 31882771. Lower Levels.
Ergothioneine Levels. Evidence: 9/10. Source: PMID 35050183. Higher Levels.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Standard transporter activity ensures efficient uptake of L-carnitine and related acylcarnitines into tissues [1]. This robust transport supports cellular energy production and helps protect red blood cells from premature breakdown [1]. Clinical studies show that this genotype is associated with a typical, baseline risk of side effects when undergoing chemotherapy with doxorubicin or cyclophosphamide [2]. While blood sugar markers like HbA1c may trend slightly higher, overall metabolic transport remains highly efficient [3]. Maintaining a balanced diet rich in natural antioxidants supports general cellular health. Knowing this status is particularly useful if planning cancer treatments or evaluating metabolic profiles.
Typical chemotherapy side effect risk; Optimal red blood cell stability.
Sample genotype: AG (Heterozygous)
Having one copy of the threonine variant leads to a moderate reduction in carnitine transporter activity [1]. This slight functional change can alter how the body processes specific medications, particularly doxorubicin and cyclophosphamide [2]. Clinical data suggests a moderately increased likelihood of experiencing drug-induced toxicity during these treatments [2]. Red blood cell stability and circulating acylcarnitine levels typically remain within normal ranges under standard conditions [3]. Blood sugar markers like HbA1c may also show a slight downward trend compared to the major genotype [4]. Discussing these genetic tendencies with a healthcare provider can help tailor wellness and treatment plans. This information is most relevant during oncology treatment planning or metabolic evaluations.
Moderately increased chemotherapy toxicity risk; Intermediate carnitine transport levels.
Sample genotype: GG (Homozygous)
Carrying two copies of the variant allele markedly reduces the efficiency of the SLC22A16 transporter [1]. This functional deficit leads to significantly lower levels of circulating acylcarnitines, which are crucial for cellular energy [2]. Research indicates that red blood cells in these individuals may exhibit reduced structural stability and increased susceptibility to oxidative stress [1]. Furthermore, clinical studies associate this genotype with a higher risk of severe toxicity and side effects when treated with doxorubicin or cyclophosphamide [3]. On the positive side, these individuals often present with slightly lower HbA1c levels and higher levels of the antioxidant ergothioneine. Sharing these insights with a medical team can assist in personalizing therapeutic strategies. This genotype is highly relevant for anyone undergoing chemotherapy or managing metabolic health.
Higher risk of chemotherapy side effects; Reduced red blood cell stability under stress.
Variants with shared genetic architecture
rs75017182 · DPYD Gene · Chr 1 · Chemotherapy Drug Toxicity
rs17376848 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
rs1801159 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
Genomic atlas of the plasma metabolome prioritizes metabolites implicated in human diseases.
Content updated August 2026.
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