FLT3 rs1933437: What Your Genotype Means
The rs1933437 variant is a genetic change in the FLT3 gene that results in a Thr227Met amino acid substitution. It is currently being studied for its potential role in influencing how individuals respond to certain tyrosine kinase inhibitor therapies.
What each genotype means
Common FLT3 variant profile
This genotype represents the homozygous state for the major allele at this position. Research into this specific FLT3 variant is currently limited, and its clinical significance regarding tyrosine kinase inhibitor therapy remains under investigation. Please discuss any concerns regarding medication response or treatment planning with your clinician or pharmacist.
This is the most common genotype in many global populations, though it is less frequent in South Asian populations where the alternative allele is highly prevalent.
Heterozygous FLT3 variant profile
You carry one copy of each allele at this FLT3 position. The functional impact of this missense variant on FLT3 receptor activity and its potential influence on tyrosine kinase inhibitor therapy is not yet fully established in clinical practice. You should consult with your healthcare provider or pharmacist to understand how this information relates to your specific medical context.
This genotype is frequently observed in populations with high minor allele frequency, particularly among individuals of South Asian ancestry.
Homozygous variant FLT3 profile
This genotype indicates you are homozygous for the minor allele at this FLT3 position. While this variant is highly prevalent in certain populations, its specific role in altering responsiveness to tyrosine kinase inhibitor therapy is still considered to have limited evidence. Always discuss your genetic findings and any potential implications for medication dosing with your clinical team.
This genotype is highly prevalent in South Asian populations, where the minor allele frequency is approximately 0.85.
Understanding the rs1933437 Variant
The rs1933437 variant is a single nucleotide polymorphism (SNP) located within the FLT3 gene. Specifically, this variant causes a missense mutation, meaning it changes the genetic code to produce a different amino acid—threonine to methionine—at position 227 in the protein sequence. This change occurs in the extracellular domain of the FLT3 receptor. In genomics, SNPs like rs1933437 are points of variation where a single letter in the DNA sequence differs between individuals. While many such variants have no observable effect, researchers track them to see if they alter protein structure or function in ways that might influence health or drug metabolism. Because this variant sits in a region of the receptor involved in ligand binding, scientists are interested in whether this structural change impacts the receptor's ability to interact with its environment or respond to therapeutic agents.
The Role of the FLT3 Gene
The FLT3 gene provides instructions for making a protein called fms-related receptor tyrosine kinase 3. This protein is a type of receptor found on the surface of certain cells, particularly those in the bone marrow that develop into blood cells. Under normal conditions, the FLT3 receptor helps regulate the growth, survival, and differentiation of these blood-forming cells. When a specific signaling molecule binds to the receptor, it triggers a cascade of signals inside the cell that promotes healthy development. However, the FLT3 gene is well-known in oncology because mutations in this gene can lead to the receptor being 'always on,' or constitutively activated. This uncontrolled signaling is a hallmark of certain hematologic malignancies, such as acute myeloid leukemia. Because of its central role in cell signaling, FLT3 is a major target for drug development, and researchers are constantly investigating how different genetic variations within this gene might affect the efficacy of targeted treatments.
Research and Clinical Evidence
The evidence linking rs1933437 to clinical outcomes is currently classified as limited. While the variant is documented in genomic databases, its functional impact on drug response is not yet fully established in large-scale clinical trials. Some research explores whether this specific missense variant alters the binding or efficacy of tyrosine kinase inhibitors, which are drugs designed to block the signaling of receptors like FLT3. However, it is important to distinguish this variant from the well-characterized, high-impact mutations like FLT3-ITD, which are known to drive leukemia progression. Because the evidence for rs1933437 is still emerging, it is not currently used as a standard clinical marker for making treatment decisions. Researchers continue to investigate whether this variant acts as a modifier of drug response, but these findings are preliminary and require further validation before they can be applied in a clinical setting.
What This Information Means for You
If you have received information about your rs1933437 genotype, it is important to understand that this is a research-level finding rather than a diagnostic tool. Genetic variants in pharmacogenomics are complex, and a single SNP rarely determines a person's entire response to a medication. Many factors, including other genetic markers, environmental influences, and the specific nature of a medical condition, play a much larger role in how a patient responds to therapy. You should never use this information to make decisions about your health or medication regimen. If you are concerned about how a specific drug might affect you, or if you are curious about the role of your genetics in your treatment plan, the best course of action is to discuss these results with your clinician or a pharmacist. They can provide context based on your full medical history and the most current, evidence-based clinical guidelines.
How common is this variant?
The minor allele frequency for rs1933437 is approximately 0.35 globally, though it shows significant variation, reaching a prevalence of about 0.85 in South Asian populations.
Frequently asked questions
Is rs1933437 a cause of leukemia?
No, rs1933437 is a common genetic variant and is not considered a driver mutation for leukemia. It is distinct from the high-impact FLT3 mutations, such as internal tandem duplications (ITD), that are known to contribute to the development of acute myeloid leukemia.
Should I change my medication based on this result?
Absolutely not. You should never change your medication or dosage based on a genetic report without consulting your doctor. Pharmacogenomic results are only one piece of a complex clinical puzzle that your healthcare provider must evaluate.
Why is the frequency of this variant so high in South Asians?
Genetic variants often reach different frequencies in different populations due to historical migration patterns, genetic drift, or evolutionary pressures. The high frequency of this variant in South Asian populations is a documented observation, but it does not necessarily imply a specific health risk.
Where can I find more information about FLT3?
You can find reliable, peer-reviewed information about the FLT3 gene and its role in health on resources like MedlinePlus Genetics or the National Center for Biotechnology Information (NCBI) Gene database.
Sources & further reading
Educational information only, last refreshed 9/23/2026. Not medical advice — these associations describe population statistics, not individual predictions.
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