What you carry at this position in your DNA and what research says about it.
Statin Muscle Pain Risk: 10/10 evidence, 14 publications.
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Sample genotype (not yours): T/T
Higher Risk of Statin-Induced Muscle Pain
Carrying two copies of the T allele is associated with an increased likelihood of experiencing muscle aches and intolerance when taking statin medications. It is also linked to higher baseline levels of muscle enzymes.
What this genotype means: Increased risk of statin-induced myalgia; Higher baseline creatine kinase levels; Higher baseline liver enzyme levels.
Sample genotype (not yours): C/C
Lower Risk of Statin-Induced Muscle Pain
Carrying two copies of the C allele is associated with a reduced risk of experiencing muscle aches during statin therapy and lower baseline muscle enzyme levels.
What this genotype means: Reduced risk of statin-induced myalgia; Lower baseline creatine kinase levels; Lower baseline liver enzyme levels.
Sample genotype (not yours): T/C
Moderate Risk of Statin-Induced Muscle Pain
Carrying one copy of the T allele and one copy of the C allele is associated with a moderate, intermediate risk of statin-induced muscle aches and slightly elevated muscle enzyme levels.
What this genotype means: Moderate risk of statin-induced myalgia; Moderately elevated baseline creatine kinase; Slightly elevated baseline liver enzymes.
Gene function and biological role
Gene Function: The LILRB5 gene encodes leukocyte immunoglobulin-like receptor subfamily B member 5, a cell surface receptor primarily expressed in immune cells, skeletal muscle, and the liver [1]. While its precise physiological role remains under active investigation, it is known to participate in immune system regulation and inflammatory responses [1]. Research indicates that LILRB5 may act as a scavenger receptor involved in clearing intracellular proteins and enzymes released into the bloodstream during tissue stress or damage [2]. This clearance function directly influences circulating levels of muscle-specific proteins, linking immune activity to muscle health [2]. Consequently, genetic variations in this gene can alter how the body processes muscle strain and responds to certain medications [1].
Variant Impact: The rs12975366 variant is a missense mutation in the LILRB5 gene that causes an aspartic acid to glycine substitution at position 247 of the protein, commonly referred to as p.Asp247Gly. This structural alteration is hypothesized to modify the receptor's binding affinity or clearance efficiency for circulating enzymes [1]. The ancestral T allele encodes the reference aspartate residue, which is associated with higher baseline levels of muscle enzymes [2]. Conversely, the variant C allele encodes glycine, resulting in more rapid clearance or lower production of these enzymes [2]. This single amino acid change has emerged as a key genetic marker for muscle-related side effects during cholesterol-lowering therapy [1].
Key Insight: This genetic variant affects statin tolerance through an immune system pathway rather than direct muscle metabolism, and it also regulates baseline muscle enzyme levels even in people who do not take statins.
Location: LILRB5. Chromosome 19 · 19q13.42 · 54.3 Mb
Estimated prevalence by population
Global 46.8%; European 34.1%; African 68.2%; East Asian 81.9%; South Asian 38.8%; Americas 46.2%; Ashkenazi 29.6%; Finnish 40.6%; Middle Eastern 22.7%; Amish 27.7%.
Estimated TT genotype frequency.
Global 41.4%; European 48.6%; African 28.8%; East Asian 17.2%; South Asian 47.0%; Americas 43.5%; Ashkenazi 49.6%; Finnish 46.2%; Middle Eastern 49.9%; Amish 49.9%.
Estimated TC genotype frequency.
Global 11.9%; European 17.3%; African 3.0%; East Asian 0.9%; South Asian 14.2%; Americas 10.3%; Ashkenazi 20.8%; Finnish 13.1%; Middle Eastern 27.4%; Amish 22.4%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Pharmacogenomics
Adverse Drug Reactions
Statin Side Effects. Evidence: 5/10. Source: PMID 29020356. Increased Risk.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Creatine Kinase Levels. Evidence: 10/10. Source: PMID 26838040. Elevated Levels.
LDH Enzyme Levels. Evidence: 8/10. Source: PMID 26838040. Elevated Levels.
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Higher Levels.
Triglycerides. Evidence: 8/10. Source: PMID 39024449. Typical Levels.
Organ Systems
Liver Function & Disease
AST Liver Enzyme. Evidence: 8/10. Source: PMID 34594039. Elevated Levels.
Showing effects for C/C genotype
Statin Side Effects. Evidence: 5/10. Source: PMID 29020356. Reduced Risk.
Creatine Kinase Levels. Evidence: 10/10. Source: PMID 26838040. Lower Levels.
LDH Enzyme Levels. Evidence: 8/10. Source: PMID 26838040. Lower Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Typical Levels.
Triglycerides. Evidence: 8/10. Source: PMID 39024449. Higher Levels.
AST Liver Enzyme. Evidence: 8/10. Source: PMID 34594039. Lower Levels.
Showing effects for T/C genotype
Statin Side Effects. Evidence: 5/10. Source: PMID 29020356. Moderate Risk.
Creatine Kinase Levels. Evidence: 10/10. Source: PMID 26838040. Moderately Elevated.
LDH Enzyme Levels. Evidence: 8/10. Source: PMID 26838040. Moderately Elevated.
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Moderately Higher.
Triglycerides. Evidence: 8/10. Source: PMID 39024449. Moderately Higher.
AST Liver Enzyme. Evidence: 8/10. Source: PMID 34594039. Moderately Elevated.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Having two copies of the T allele, which encodes the reference aspartate residue, is associated with a significantly higher risk of statin-induced myalgia and general statin intolerance [1]. Clinical studies show that these individuals have higher baseline levels of creatine kinase and lactate dehydrogenase, which are classic biomarkers of muscle strain or damage [2]. When prescribed statins, the risk of developing muscle pain or needing to switch medications due to intolerance is elevated compared to those with the C allele [1]. This genetic profile is also associated with higher levels of aspartate aminotransferase, a liver and muscle enzyme [3]. Interestingly, this genotype is linked to higher levels of beneficial HDL cholesterol [4]. Despite the increased risk of muscle symptoms, statins remain highly effective for cardiovascular protection.
Increased risk of statin-induced myalgia; Higher baseline creatine kinase levels; Higher baseline liver enzyme levels.
Sample genotype: CC (Homozygous)
Having two copies of the C allele, which encodes the variant glycine residue, is highly protective against statin-induced myalgia and statin intolerance [1]. Clinical cohorts demonstrate that individuals with this genotype have significantly lower baseline levels of creatine kinase and lactate dehydrogenase, indicating lower muscle-related enzyme release or faster clearance [2]. This protective effect makes it much easier to tolerate standard statin therapies without experiencing limiting muscle aches [1]. Additionally, this genotype is associated with lower levels of the liver and muscle enzyme aspartate aminotransferase [3]. However, it is also linked to slightly lower levels of HDL cholesterol and higher levels of triglycerides [4]. Despite these minor lipid trade-offs, the overall reduction in muscle-related side effects represents a major clinical advantage for cardiovascular management.
Reduced risk of statin-induced myalgia; Lower baseline creatine kinase levels; Lower baseline liver enzyme levels.
Sample genotype: TC (Heterozygous)
Having one copy of each allele results in an intermediate phenotype for muscle enzyme levels and statin tolerance [1]. Individuals with this genotype have a moderate risk of experiencing statin-associated muscle symptoms compared to those with the protective C/C genotype [1]. Baseline levels of creatine kinase and lactate dehydrogenase are typically higher than in C/C individuals but lower than in T/T individuals [2]. This intermediate status also extends to circulating levels of aspartate aminotransferase [3]. On the lipid front, this genotype is associated with a moderate increase in HDL cholesterol compared to the C/C genotype [4]. Understanding this genetic predisposition can help guide discussions about cardiovascular therapy options and monitoring strategies. It highlights the role of immunogenetic factors in determining how muscles respond to lipid-lowering drugs.
Moderate risk of statin-induced myalgia; Moderately elevated baseline creatine kinase; Slightly elevated baseline liver enzymes.
Variants with shared genetic architecture
rs4149056 · SLCO1B1 Gene · Chr 12 · Statin Side Effect Risk
rs1801690 · APOH Gene · Chr 17 · Thyroid and Heart Health
rs11045819 · SLCO1B1 Gene · Chr 12 · Statin Response
A common missense variant of LILRB5 is associated with statin intolerance and myalgia.
Common and rare variants associating with serum levels of creatine kinase and lactate dehydrogenase.
A cross-population atlas of genetic associations for 220 human phenotypes.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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