Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement: genes and variants

Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement is linked to 1 analyzed protein (TUBB3). 6 DNA variants are known to cause it; 4 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 Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement

Known disease-causing variants in Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement

VariantPositionProtein partClinical label
TUBB3 R262C262Disease-causing (★★★★)
TUBB3 A302T302Disease-causing (★★)
TUBB3 R262H262Disease-causing (★★)
TUBB3 V175L175Disease-causing (★★)
TUBB3 S78L78Disease-causing (★)
TUBB3 D417H417Disease-causing

Same protein, different disease

Diseases related to Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement

Frequently asked questions

Which genes are linked to Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement?

In CATVariant, Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement is linked to 1 analyzed protein: TUBB3 (Tubulin beta-3 chain).

How many genetic variants are linked to Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement?

18 variants: 6 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 4 are of uncertain significance or have conflicting reports.

Which uncertain variants in Fibrosis of extraocular muscles, congenital, 3A, with or without extraocular involvement 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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