G6PD rs6791924: What Your Genotype Means
The rs6791924 single nucleotide polymorphism is a coding variant located within the X-linked G6PD gene. This variant has been investigated for its association with glucose-6-phosphate dehydrogenase deficiency, a condition that can impair red blood cell stability under chemical stress. Carrying certain risk alleles at this locus may increase susceptibility to acute hemolytic anemia following exposure to oxidative triggers, such as fava beans or specific medications including rasburicase and primaquine.
What each genotype means
Normal enzyme activity
You carry two copies of the reference C allele, which is associated with typical glucose-6-phosphate dehydrogenase (G6PD) enzyme function. Research indicates individuals with this genotype are generally not at elevated inherited risk for acute hemolytic anemia from oxidative triggers. Always review medications and dosing decisions directly with your physician or pharmacist.
Found in the vast majority of people worldwide, including more than 90% of individuals across most non-Mediterranean populations.
Variable enzyme activity
You carry one copy of the variant T allele, which confers reduced G6PD enzyme stability. Because the G6PD gene is located on the X chromosome, females with one variant copy can exhibit variable G6PD activity due to random X-chromosome inactivation, ranging from normal to deficient. If you are prescribed oxidative medications such as rasburicase or primaquine, discuss pre-treatment quantitative enzyme testing with your healthcare provider.
Carried by approximately 5% to 15% of females in Mediterranean, Middle Eastern, and North African populations, but rare in East Asian and northern European groups.
G6PD deficiency
You carry two copies of the variant T allele (or a single copy if hemizygous on the X chromosome), which is strongly associated with G6PD deficiency and markedly reduced enzyme function. In population and clinical studies, this genotype confers a significant risk of acute hemolytic anemia when exposed to oxidative triggers, including fava beans, certain infections, and hemolytic medications like rasburicase or primaquine. Consult your clinician or pharmacist to discuss safer medication alternatives and enzyme monitoring before taking potential oxidative agents.
Carried by roughly 5% to 10% of males (as a hemizygous single T allele) and less than 1% to 2% of homozygous females in Mediterranean and Middle Eastern populations, while very rare elsewhere.
Understanding rs6791924 and the G6PD Gene
The rs6791924 polymorphism is situated on the human X chromosome within the glucose-6-phosphate dehydrogenase (G6PD) gene. Because G6PD is located on the X chromosome (Xq28), genetic variation at this locus follows an X-linked inheritance pattern. Males possess only one X chromosome and are hemizygous, meaning carrying a single variant allele dictates their cellular genetic coding for this site. In contrast, females carry two X chromosomes and may be homozygous or heterozygous. Due to lyonization, also known as random X-chromosome inactivation, heterozygous females have mosaic cell populations where red blood cells express either the maternal or paternal G6PD allele. The G6PD gene encodes an essential housekeeping enzyme that protects cells from oxidative damage, particularly red blood cells, which lack a nucleus and mitochondria to regenerate proteins once mature.
Biological Function: The Role of G6PD in Red Blood Cells
Glucose-6-phosphate dehydrogenase functions as the rate-limiting enzyme in the pentose phosphate pathway, catalyzing the oxidation of glucose-6-phosphate to 6-phosphoglucono-delta-lactone while reducing NADP+ to NADPH. For mature erythrocytes, G6PD represents the sole cellular mechanism for generating NADPH. In turn, NADPH is required to regenerate reduced glutathione, a vital intracellular antioxidant that neutralizes reactive oxygen species and safeguards hemoglobin, red blood cell enzymes, and cell membrane lipids from oxidative stress. If a genetic alteration diminishes the structural stability or catalytic efficiency of G6PD, red blood cells become exceptionally vulnerable to oxidative damage. When exposed to oxidizing agents, red blood cells can undergo rapid destruction, known as acute hemolysis, leading to hemolytic anemia, hemoglobinuria, and hyperbilirubinemia.
Clinical and Pharmacogenomic Evidence
Evidence linking rs6791924 to clinically relevant G6PD deficiency and drug-induced hemolysis is currently categorized as limited. Pharmacogenomics research, including clinical guidelines from organizations such as the Clinical Pharmacogenetics Implementation Consortium (CPIC), highlights that individuals with diminished G6PD activity face severe hemolytic risks when exposed to high-risk oxidizing medications. Notable examples include rasburicase (used for tumor lysis syndrome) and primaquine or tafenoquine (used in antimalarial therapy). While specific classic variants such as G6PD Mediterranean (c.563C>T) or G6PD A- (c.202G>A, c.376A>G) are well-characterized high-risk alleles, rs6791924 is associated with moderate or variable decreases in enzyme stability. Because evidence for rs6791924 remains limited and population-specific, biochemical enzyme assays remain the gold standard for assessing clinical hemolysis risk rather than relying solely on this single marker.
What You Can and Cannot Do With This Information
Identifying an rs6791924 variant in direct-to-consumer genetic testing does not constitute a clinical diagnosis of G6PD deficiency, nor does it guarantee you will experience adverse drug reactions. Due to limited clinical evidence and the variable expression of X-linked traits in females, a genetic test alone is insufficient to guide therapeutic decisions. Never stop, initiate, or adjust the dosage of any prescribed medication, including antimalarials, uric acid agents, or sulfa drugs, based on a genetic read-out. If you carry a variant allele or have a personal or family history of unexplained jaundice, dark urine, or hemolytic anemia, consult a healthcare provider or genetic counselor. A simple, standardized biochemical G6PD enzyme activity blood test can accurately determine your functional enzyme levels and clarify your medical safety profile.
How common is this variant?
The variant allele at rs6791924 is polymorphic in Mediterranean, Middle Eastern, and North African populations, occurring at frequencies between roughly 0.05 and 0.10, while remaining uncommon in most other ancestral backgrounds.
Frequently asked questions
What is rs6791924?
rs6791924 is a single nucleotide polymorphism located in the G6PD gene on the X chromosome. It has been studied for its potential role in glucose-6-phosphate dehydrogenase deficiency and susceptibility to acute hemolytic anemia under oxidative stress.
Does having the rs6791924 variant mean I have G6PD deficiency?
Not necessarily. Evidence directly linking rs6791924 to severe deficiency is limited, and female carriers may display normal enzyme activity due to random X-chromosome inactivation. Only a functional blood test measuring G6PD enzyme levels can clinically diagnose G6PD deficiency.
Can I take medications like primaquine if I have this variant?
You should never modify or avoid medications without professional guidance. CPIC guidelines recommend screening G6PD functional enzyme activity prior to prescribing high-risk drugs like primaquine or rasburicase. Discuss any genetic findings with your physician or pharmacist so they can evaluate your functional enzyme status.
Why does G6PD deficiency affect men and women differently?
The G6PD gene is located on the X chromosome. Because men have only one X chromosome, possessing a single altered allele affects all of their red blood cells. Women have two X chromosomes, so X-inactivation creates a mosaic where only a portion of their red cells may express the deficient enzyme.
Sources & further reading
Educational information only, last refreshed 9/13/2026. Not medical advice — these associations describe population statistics, not individual predictions.
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Known as the G6PD A+ variant (p.Asn126Asp), this polymorphism is common in African populations. While it does not cause G6PD deficiency on its own, it is a component of the G6PD A- haplotype, which is associated with reduced enzyme stability and clinical deficiency.
Causes the A- variant of G6PD deficiency, common in African populations.
Causes G6PD deficiency and favism risk in Mediterranean populations.
This variant is associated with G6PD deficiency, which can lead to hemolytic anemia upon exposure to certain medications or fava beans.
This variant is a known genetic contributor to G6PD deficiency, impacting drug metabolism and sensitivity to oxidative stress.
This variant is associated with G6PD deficiency, which can lead to hemolytic anemia when exposed to certain medications or stressors.