The protein is predicted to function as a DNA-binding transcription factor that regulates gene expression by RNA polymerase II and is involved in anatomical structure development and cell differentiation. Mutations in this gene have not been definitively associated with human disease in pediatric populations. The gene appears to be tolerant to loss-of-function variants based on constraint metrics.

OMIMResearchSummary from RefSeq, UniProt
DNmechanismLOEUF 1.85
Clinical SummaryFOXI2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.85LOEUF
pLI 0.000
Z-score -0.17
OE 1.09 (0.551.85)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.09Z-score
OE missense 1.02 (0.891.18)
139 obs / 136.0 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.09 (0.551.85)
00.351.4
Missense OE1.02 (0.891.18)
00.61.4
Synonymous OE1.14
01.21.6
LoF obs/exp: 5 / 4.6Missense obs/exp: 139 / 136.0Syn Z: -0.88
DN
0.6745th %ile
GOF
0.5857th %ile
LOF
0.56top 25%

The highest-scoring mechanism for this gene is dominant-negative.

DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

FOXI2 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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