Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations: genes and variants

Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations is linked to 1 analyzed protein (TREX1). 3 DNA variants are known to cause it; 249 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 Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations

Known disease-causing variants in Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations

VariantPositionProtein partClinical label
TREX1 R114H114Disease-causing (★★★★)
TREX1 D18N18Disease-causing (★★)
TREX1 D200N200Disease-causing (★)

Diseases related to Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations

Frequently asked questions

Which genes are linked to Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations?

In CATVariant, Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations is linked to 1 analyzed protein: TREX1 (Three-prime repair exonuclease 1).

How many genetic variants are linked to Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations?

276 variants: 3 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 249 are of uncertain significance or have conflicting reports.

Which uncertain variants in Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations 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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