What you carry at this position in your DNA and what research says about it.
Fetal Hemoglobin Levels: 8/10 evidence, 18 publications.
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Sample genotype (not yours): A/A
Typical Fetal Hemoglobin Levels
This genotype is associated with standard baseline levels of fetal hemoglobin in adult blood. It represents the most common genetic profile globally.
What this genotype means: Standard adult hemoglobin transition; Typical baseline blood cell counts.
Sample genotype (not yours): A/G
Increased Fetal Hemoglobin Levels
Carrying one copy of the G allele is linked to higher adult levels of fetal hemoglobin. This can provide a protective effect against certain blood disorders.
What this genotype means: Persistent adult fetal hemoglobin production; Milder symptoms in inherited blood disorders.
Sample genotype (not yours): G/G
Highest Fetal Hemoglobin Levels
Carrying two copies of the G allele is associated with the highest persistence of fetal hemoglobin in adulthood. This provides the strongest protective buffer against red blood cell disorders.
What this genotype means: Maximum persistence of adult fetal hemoglobin; Strongest genetic protection against red blood cell sickling.
Gene function and biological role
Gene Function: The HBS1L-MYB intergenic region on chromosome 6 acts as a critical regulatory hub controlling the transition from fetal to adult hemoglobin. This region contains enhancer elements that modulate the expression of the neighboring MYB gene, which is a master regulator of red blood cell development [1]. Variations in this genomic area alter the binding of transcription factors, directly impacting how long the body continues to produce fetal hemoglobin into adulthood [2]. Higher levels of fetal hemoglobin can act as a natural buffer against the clinical severity of inherited red blood cell disorders [3]. Additionally, this locus plays a broader role in regulating the production and maturation of multiple blood cell lineages, including platelets and white blood cells [4].
Variant Impact: The rs4895441 variant is located in the upstream regulatory region of the HBS1L-MYB locus, where it influences the expression of genes involved in hematopoiesis. The G allele of this variant is associated with increased persistence of fetal hemoglobin in adult red blood cells [1]. This genetic change also correlates with alterations in other hematological traits, such as higher platelet counts and lower white blood cell counts [5]. By modifying the transcriptional activity of the MYB gene, the variant shifts the balance of blood cell differentiation in the bone marrow [2]. These downstream effects have been shown to influence clinical outcomes and disease severity in individuals with hemoglobin disorders [3].
Key Insight: The G allele acts as a natural genetic modifier that helps maintain fetal hemoglobin production into adulthood, which can significantly reduce the severity of certain inherited blood conditions.
Location: HBS1L. Chromosome 6 · 6q23.3 · 135.1 Mb
Estimated prevalence by population
Global 62.6%; European 53.5%; African 81.6%; East Asian 51.7%; South Asian 79.2%; Americas 64.6%; Ashkenazi 58.1%; Finnish 42.5%; Middle Eastern 63.9%; Amish 65.6%.
Estimated AA genotype frequency.
Global 32.2%; European 39.3%; African 17.5%; East Asian 40.4%; South Asian 19.6%; Americas 31.6%; Ashkenazi 36.3%; Finnish 45.4%; Middle Eastern 32.1%; Amish 30.8%.
Estimated AG genotype frequency.
Global 5.2%; European 7.2%; African 0.9%; East Asian 7.9%; South Asian 1.2%; Americas 3.9%; Ashkenazi 5.7%; Finnish 12.1%; Middle Eastern 4.0%; Amish 3.6%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Rare Genetic Disorders
Hemoglobinopathies
Fetal Hemoglobin. Evidence: 4/10. Source: PMID 25806420. Typical Levels.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Platelet Count. Evidence: 6/10. Source: PMID 26805783. Typical Count.
White Blood Cell Count. Evidence: 6/10. Source: PMID 20139978. Higher Count.
Lifestyle, Fitness & Aging
Aging & Longevity
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Typical Abundance.
Showing effects for A/G genotype
Fetal Hemoglobin. Evidence: 4/10. Source: PMID 25806420. Increased Levels.
Platelet Count. Evidence: 6/10. Source: PMID 26805783. Slightly Higher.
White Blood Cell Count. Evidence: 6/10. Source: PMID 20139978. Slightly Lower.
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Slightly Higher.
Showing effects for G/G genotype
Fetal Hemoglobin. Evidence: 4/10. Source: PMID 25806420. Highest Levels.
Platelet Count. Evidence: 6/10. Source: PMID 26805783. Higher Count.
White Blood Cell Count. Evidence: 6/10. Source: PMID 20139978. Lower Count.
Mitochondrial DNA Copy Number. Evidence: 8/10. Source: PMID 33385171. Higher Abundance.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Adults with this genotype typically transition fully from fetal hemoglobin to adult hemoglobin during infancy, leaving only trace amounts of the fetal form in circulation [1]. While this is the standard biological progression, it means there is no additional genetic buffer against red blood cell stressors [2]. Clinical studies show that individuals with this profile experience typical baseline rates of blood cell production across red cells, white cells, and platelets [3]. In the context of inherited hemoglobin disorders, this genotype is associated with standard clinical presentation rather than the milder symptoms seen in carriers of the protective variant [4].
Standard adult hemoglobin transition; Typical baseline blood cell counts.
Sample genotype: AG (Heterozygous)
Inheriting a single copy of the G allele alters the regulatory activity of the HBS1L-MYB region, allowing the body to continue producing moderate amounts of fetal hemoglobin into adulthood [1]. This persistent fetal hemoglobin can help stabilize red blood cells and improve oxygen transport under stress [2]. Research indicates that this genotype is associated with a milder clinical course and fewer complications in individuals with sickle cell disease or beta-thalassemia [3]. Additionally, this profile is linked to slight shifts in other blood parameters, including a modest increase in platelet count and a slight reduction in white blood cell count [4].
Persistent adult fetal hemoglobin production; Milder symptoms in inherited blood disorders.
Sample genotype: GG (Homozygous)
Having two copies of the G allele significantly modifies the expression of the MYB gene, leading to the highest levels of adult fetal hemoglobin production among the genotypes [1]. This elevated fetal hemoglobin acts as a powerful natural defense mechanism that can dramatically ameliorate the severity of hemoglobinopathies [2]. Clinical cohorts show that individuals with this genetic profile experience fewer pain crises and reduced transfusion requirements when affected by red blood cell disorders [3]. The genotype also influences broader hematological traits, resulting in higher platelet counts, increased mitochondrial DNA copy number in blood cells, and lower white blood cell counts [4].
Maximum persistence of adult fetal hemoglobin; Strongest genetic protection against red blood cell sickling.
Variants with shared genetic architecture
rs9376090 · HBS1L Gene · Chr 6 · Blood and Heart Health
rs7775698 · HBS1L Gene · Chr 6 · Fetal Hemoglobin Levels
rs9402686 · HBS1L Gene · Chr 6 · Fetal Hemoglobin Levels
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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