What you carry at this position in your DNA and what research says about it.
Fatty Liver Disease Risk: 8/10 evidence, 22 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): C/C
Typical Risk of Fatty Liver Disease
Possession of two C alleles is associated with normal MBOAT7 enzyme levels and typical liver fat accumulation. This genetic profile provides relative protection against progressive liver inflammation and fibrosis compared to T allele carriers.
What this genotype means: Normal MBOAT7 enzyme expression; Typical liver fat accumulation; Lower risk of liver fibrosis.
Sample genotype (not yours): C/T
Increased Risk of Fatty Liver Disease
Presence of one T allele is linked to reduced MBOAT7 enzyme expression and a higher risk of liver fat accumulation. This genetic profile moderately increases the susceptibility to liver inflammation and progressive fibrosis.
What this genotype means: Reduced MBOAT7 enzyme expression; Increased liver fat accumulation; Higher risk of liver fibrosis.
Sample genotype (not yours): T/T
Highest Risk of Fatty Liver Disease
Possession of two T alleles is associated with the lowest levels of MBOAT7 expression and the highest risk of liver fat accumulation. This genetic profile significantly increases susceptibility to liver inflammation, fibrosis, and cirrhosis.
What this genotype means: Lowest MBOAT7 enzyme expression; Highest liver fat accumulation; Greatest risk of liver fibrosis and cirrhosis.
Gene function and biological role
Gene Function: The MBOAT7 gene encodes lysophosphatidylinositol acyltransferase 1, an enzyme crucial for lipid remodeling in cell membranes. It specifically incorporates polyunsaturated fatty acids like arachidonic acid into phosphatidylinositols. This process, known as the Lands cycle, maintains the precise lipid composition of cellular membranes, particularly in the liver. When this gene is less active, the liver cannot properly process these lipids, leading to abnormal fat accumulation. Over time, this lipid imbalance triggers cellular stress and inflammation in hepatic tissues.
Variant Impact: The rs641738 variant is a single nucleotide change located in the MBOAT7-TMC4 locus on chromosome 19. The T allele of this variant is associated with significantly reduced expression of the MBOAT7 protein in liver tissue [1]. This reduction in enzyme levels compromises the remodeling of phosphatidylinositol lipids, altering hepatic lipid composition [1]. Consequently, individuals carrying the T allele are more susceptible to fat accumulation in the liver [1]. This genetic change acts as a key predisposing factor for progressive liver damage [2].
Key Insight: Carrying the T allele reduces the liver's ability to remodel essential membrane lipids, which directly promotes fat accumulation. Interestingly, while the T allele increases liver disease risk, some studies suggest it may associate with a slightly reduced risk of cardiovascular events.
Location: MBOAT7. Chromosome 19 · 19q13.42 · 54.2 Mb
Estimated prevalence by population
Global 37.4%; European 31.7%; African 44.1%; East Asian 57.3%; South Asian 23.0%; Americas 40.7%; Ashkenazi 46.2%; Finnish 37.2%; Middle Eastern 29.6%; Amish 42.4%.
Estimated CC genotype frequency.
Global 47.0%; European 49.2%; African 44.6%; East Asian 36.8%; South Asian 49.9%; Americas 46.2%; Ashkenazi 43.5%; Finnish 47.6%; Middle Eastern 49.6%; Amish 45.4%.
Estimated CT genotype frequency.
Global 15.6%; European 19.1%; African 11.3%; East Asian 5.9%; South Asian 27.1%; Americas 13.1%; Ashkenazi 10.3%; Finnish 15.2%; Middle Eastern 20.8%; Amish 12.2%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Liver Function & Disease
Fatty Liver Disease. Evidence: 3/10. Source: PMID 26850495. Typical Risk.
Liver Fibrosis. Evidence: 3/10. Source: PMID 30875804. Typical Risk.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Platelet Count. Evidence: 8/10. Source: PMID 32888493. Typical.
Lipids & Cholesterol
Phospholipid Levels. Evidence: 6/10. Source: PMID 35050183. Typical.
Showing effects for C/T genotype
Fatty Liver Disease. Evidence: 3/10. Source: PMID 26850495. Increased Risk.
Liver Fibrosis. Evidence: 3/10. Source: PMID 30875804. Increased Risk.
Platelet Count. Evidence: 8/10. Source: PMID 32888493. Slightly Higher.
Phospholipid Levels. Evidence: 6/10. Source: PMID 35050183. Altered Levels.
Showing effects for T/T genotype
Fatty Liver Disease. Evidence: 3/10. Source: PMID 26850495. Highest Risk.
Liver Fibrosis. Evidence: 3/10. Source: PMID 30875804. Highest Risk.
Platelet Count. Evidence: 8/10. Source: PMID 32888493. Higher.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Inheriting the C/C genotype means possessing two copies of the typical, fully functional allele. This genetic profile ensures normal expression of the MBOAT7 enzyme in the liver [1]. Consequently, the liver can efficiently remodel phosphatidylinositol lipids, preventing the abnormal accumulation of triglycerides [1]. Studies show that individuals with this genotype have a lower baseline risk of developing nonalcoholic fatty liver disease [1]. Furthermore, they are at a lower risk for progressive liver complications such as fibrosis and cirrhosis [2]. Maintaining a balanced diet and limiting alcohol intake helps preserve this natural hepatic protection. Regular physical activity also supports overall metabolic and liver health.
Normal MBOAT7 enzyme expression; Typical liver fat accumulation; Lower risk of liver fibrosis.
Sample genotype: CT (Heterozygous)
Carriage of the C/T genotype means carrying one copy of the risk-associated T allele. This genetic setup leads to a moderate reduction in MBOAT7 enzyme levels in liver tissue [1]. With lower enzyme activity, the liver's ability to remodel membrane phospholipids is compromised, promoting triglyceride retention [1]. Clinical studies have linked this genotype to an increased risk of developing nonalcoholic fatty liver disease [1]. Additionally, carriers show a higher susceptibility to progressive liver damage, including inflammation and fibrosis [2]. Managing metabolic risk factors is particularly beneficial for individuals with this genotype. Minimizing alcohol consumption and maintaining a healthy weight can help mitigate the genetic predisposition to liver fat accumulation.
Reduced MBOAT7 enzyme expression; Increased liver fat accumulation; Higher risk of liver fibrosis.
Sample genotype: TT (Homozygous)
Inheriting the T/T genotype means possessing two copies of the risk allele, resulting in the lowest levels of MBOAT7 enzyme expression in the liver [1]. This severe reduction in enzyme activity significantly impairs the remodeling of phosphatidylinositol lipids, leading to marked triglyceride accumulation in hepatic cells [1]. Research indicates that individuals with this genotype have a substantially higher risk of nonalcoholic fatty liver disease [1]. They are also at the greatest risk for progressive liver complications, including severe fibrosis and cirrhosis [2]. Lifestyle choices play a critical role in managing this genetic risk. Adopting a liver-friendly diet, avoiding alcohol, and engaging in regular exercise are highly recommended strategies to support hepatic function.
Lowest MBOAT7 enzyme expression; Highest liver fat accumulation; Greatest risk of liver fibrosis and cirrhosis.
Variants with shared genetic architecture
rs8736 · MBOAT7 Gene · Chr 19 · Fatty Liver Disease Risk
rs626283 · MBOAT7 Gene · Chr 19 · Liver Disease Risk
rs738408 · PNPLA3 Gene · Chr 22 · Fatty Liver Risk
TM6SF2 and MBOAT7 Gene Variants in Liver Fibrosis and Cirrhosis.
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