Blepharophimosis-impaired intellectual development syndrome: genes and variants

Blepharophimosis-impaired intellectual development syndrome is linked to 1 analyzed protein (SMARCA2). 8 DNA variants are known to cause it; 11 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Blepharophimosis-impaired intellectual development syndrome

Known disease-causing variants in Blepharophimosis-impaired intellectual development syndrome

VariantPositionProtein partClinical label
SMARCA2 R937H937Disease-causing (★★)
SMARCA2 R525C525Disease-causing (★★)
SMARCA2 D534G534Disease-causing (★★)
SMARCA2 R1105H1105Helicase C-terminalDisease-causing (★★)
SMARCA2 R937C937Disease-causing (★)
SMARCA2 Q957R957Disease-causing (★)
SMARCA2 P625L625Disease-causing (★)
SMARCA2 R937L937Disease-causing

Same protein, different disease

Diseases related to Blepharophimosis-impaired intellectual development syndrome

Frequently asked questions

Which genes are linked to Blepharophimosis-impaired intellectual development syndrome?

In CATVariant, Blepharophimosis-impaired intellectual development syndrome is linked to 1 analyzed protein: SMARCA2 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2).

How many genetic variants are linked to Blepharophimosis-impaired intellectual development syndrome?

28 variants: 8 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 11 are of uncertain significance or have conflicting reports.

Which uncertain variants in Blepharophimosis-impaired intellectual development syndrome look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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