Autosomal dominant vitreoretinochoroidopathy: genes and variants

Autosomal dominant vitreoretinochoroidopathy is linked to 1 analyzed protein (BEST1). 9 DNA variants are known to cause it; 13 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 Autosomal dominant vitreoretinochoroidopathy

Where Autosomal dominant vitreoretinochoroidopathy variants cluster

Known disease-causing variants in Autosomal dominant vitreoretinochoroidopathy

VariantPositionProtein partClinical label
BEST1 R218C218CytoplasmicDisease-causing (★★★★)
BEST1 A195V195CytoplasmicDisease-causing (★★)
BEST1 I201T201CytoplasmicDisease-causing (★★)
BEST1 D228H228CytoplasmicDisease-causing (★★)
BEST1 F80L80TransmembraneDisease-causing (★★)
BEST1 I205T205CytoplasmicDisease-causing (★★)
BEST1 D228E228CytoplasmicDisease-causing (★)
BEST1 D303V303CytoplasmicDisease-causing (★)
BEST1 V235A235CytoplasmicDisease-causing

Same protein, different disease

Diseases related to Autosomal dominant vitreoretinochoroidopathy

Frequently asked questions

Which genes are linked to Autosomal dominant vitreoretinochoroidopathy?

In CATVariant, Autosomal dominant vitreoretinochoroidopathy is linked to 1 analyzed protein: BEST1 (Bestrophin-1).

How many genetic variants are linked to Autosomal dominant vitreoretinochoroidopathy?

31 variants: 9 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 13 are of uncertain significance or have conflicting reports.

Which uncertain variants in Autosomal dominant vitreoretinochoroidopathy 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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