What you carry at this position in your DNA and what research says about it.
Inflammatory Response: 8/10 evidence, 3 publications.
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Sample genotype (not yours): C/C
Typical Inflammatory Response
A balanced baseline immune response is typical for this genetic profile. It avoids the elevated systemic inflammation and higher white blood cell counts associated with the variant allele.
What this genotype means: Typical baseline monocyte and eosinophil counts; Balanced inflammatory cytokine production; Lower risk of inflammation-associated complications.
Sample genotype (not yours): A/A
Elevated Inflammatory Response
Elevated baseline levels of inflammatory cells and cytokines are associated with this genetic profile. A more active systemic inflammatory profile is promoted by this double-variant combination.
What this genotype means: Higher baseline monocyte and eosinophil counts; Elevated levels of circulating inflammatory cytokines; Pronounced pro-inflammatory baseline profile.
Sample genotype (not yours): C/A
Slightly Elevated Inflammatory Response
Slightly higher levels of certain white blood cells and inflammatory proteins characterize this genetic profile. A more active baseline immune response may result from this single-letter change.
What this genotype means: Slightly higher monocyte and eosinophil counts; Mildly elevated baseline inflammatory proteins; Slightly higher sensitivity to inflammatory triggers.
Gene function and biological role
Gene Function: The NLRP12 gene encodes a cytoplasmic protein that belongs to the NLR family, which plays a vital role in the immune system. This protein acts as a crucial negative regulator of inflammation, helping to suppress excessive immune responses in activated immune cells [1]. By keeping inflammatory pathways like NF-kB in check, NLRP12 helps maintain tissue homeostasis and prevents chronic inflammatory damage [1]. When NLRP12 function is compromised, the body may struggle to resolve inflammation, leading to elevated levels of pro-inflammatory cytokines [1]. Rare, severe mutations in this gene can cause familial cold autoinflammatory syndrome type 2, a condition marked by cold-induced fever and rashes [1].
Variant Impact: A single-nucleotide change in the NLRP12 gene, rs34436714, alters the amino acid at position 39 from glycine to valine. This structural change alters the protein's regulatory domain, affecting how it interacts with other immune signaling molecules [1]. The variant is associated with significant changes in the levels of circulating immune proteins, including interleukin-1 beta and S100-A9 [1] [2]. It also influences the production of key white blood cells, such as monocytes and eosinophils, which are central to the body's inflammatory response [3]. While the variant is classified as benign for rare, severe autoinflammatory syndromes, it acts as a common genetic dial that tunes baseline systemic inflammation.
Key Insight: This variant acts as a genetic dial for baseline inflammation, influencing both white blood cell counts and the release of key inflammatory cytokines without causing severe autoinflammatory disease.
Location: NLRP12. Chromosome 19 · 19q13.42 · 53.8 Mb
Estimated prevalence by population
Global 56.3%; European 62.4%; African 40.0%; East Asian 68.5%; South Asian 55.7%; Americas 58.6%; Ashkenazi 76.7%; Finnish 65.7%; Middle Eastern 69.3%; Amish 46.3%.
Estimated CC genotype frequency.
Global 36.7%; European 33.2%; African 46.5%; East Asian 28.5%; South Asian 37.8%; Americas 35.9%; Ashkenazi 21.8%; Finnish 30.7%; Middle Eastern 27.9%; Amish 43.5%.
Estimated CA genotype frequency.
Global 7.0%; European 4.4%; African 13.5%; East Asian 3.0%; South Asian 6.4%; Americas 5.5%; Ashkenazi 1.6%; Finnish 3.6%; Middle Eastern 2.8%; Amish 10.2%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Monocyte Count. Evidence: 8/10. Source: PMID 37596262. Typical.
Eosinophil Count. Evidence: 8/10. Source: PMID 37596262. Typical.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
IL-1 Beta Levels. Evidence: 8/10. Source: PMID 39789286. Typical.
S100-A9 Protein Levels. Evidence: 6/10. Source: PMID 29875488. Typical.
Showing effects for A/A genotype
Monocyte Count. Evidence: 8/10. Source: PMID 37596262. Increased.
Eosinophil Count. Evidence: 8/10. Source: PMID 37596262. Increased.
IL-1 Beta Levels. Evidence: 8/10. Source: PMID 39789286. Increased.
S100-A9 Protein Levels. Evidence: 6/10. Source: PMID 29875488. Increased.
Showing effects for C/A genotype
Monocyte Count. Evidence: 8/10. Source: PMID 37596262. Slightly Increased.
Eosinophil Count. Evidence: 8/10. Source: PMID 37596262. Slightly Increased.
IL-1 Beta Levels. Evidence: 8/10. Source: PMID 39789286. Slightly Increased.
S100-A9 Protein Levels. Evidence: 6/10. Source: PMID 29875488. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Inheriting the standard C allele from both parents ensures that the NLRP12 protein retains its typical glycine residue at position 39. Normal protein structure allows NLRP12 to function effectively as a negative regulator of inflammation, keeping immune pathways balanced. Baseline counts of monocytes and eosinophils remain within the typical range for this group [1]. Standard levels of circulating inflammatory cytokines, such as interleukin-1 beta and S100-A9, are also maintained [2] [3]. Because this profile avoids the pro-inflammatory tendency of the variant, it represents a lower risk of inflammatory complications. It serves as the standard genetic baseline for immune system regulation.
Typical baseline monocyte and eosinophil counts; Balanced inflammatory cytokine production; Lower risk of inflammation-associated complications.
Sample genotype: AA (Homozygous)
Two copies of the A allele mean that all NLRP12 proteins carry the valine substitution, which dampens their capacity to downregulate inflammatory pathways. Significantly higher baseline counts of monocytes and eosinophils are strongly associated with this profile [1]. The highest baseline levels of pro-inflammatory proteins, including interleukin-1 beta and S100-A9, are also typical [2] [3]. Although ClinVar confirms this variant is benign for rare autoinflammatory syndromes, the elevated baseline immune activity represents a more pronounced pro-inflammatory state. This genetic profile may influence how the body responds to chronic inflammatory challenges and environmental stressors. Managing overall lifestyle factors that influence inflammation can be particularly beneficial for maintaining long-term wellness.
Higher baseline monocyte and eosinophil counts; Elevated levels of circulating inflammatory cytokines; Pronounced pro-inflammatory baseline profile.
Sample genotype: CA (Heterozygous)
A single copy of the A allele introduces a valine residue in place of glycine in a portion of the NLRP12 proteins. This structural alteration slightly reduces the protein's ability to suppress inflammatory signaling pathways. Baseline counts of monocytes and eosinophils tend to be slightly higher as a result [1]. Elevated levels of circulating inflammatory markers, such as interleukin-1 beta and S100-A9, are also observed [2] [3]. While this mild increase in immune activity does not cause severe autoinflammatory diseases, it contributes to a slightly more active baseline inflammatory state. This state has been linked in clinical research to increased sensitivity to inflammatory triggers.
Slightly higher monocyte and eosinophil counts; Mildly elevated baseline inflammatory proteins; Slightly higher sensitivity to inflammatory triggers.
Variants with shared genetic architecture
rs10849448 · LTBR Gene · Chr 12 · Respiratory Infection Risk
rs1800973 · LYZ Gene · Chr 12 · Mouth Ulcer Risk
rs2239633 · CEBPE Gene · Chr 14 · Childhood Leukemia Risk
A scalable variational inference approach for increased mixed-model association power.
Genomic atlas of the human plasma proteome.
Content updated August 2026.
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