Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities: genes and variants

Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities is linked to 1 analyzed protein (BCL11B). 3 DNA variants are known to cause it; 19 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 Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities

Known disease-causing variants in Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities

VariantPositionProtein partClinical label
BCL11B N807K807C2H2-type 4Disease-causing (★★)
BCL11B K838R838C2H2-type 5Disease-causing (★)
BCL11B R841H841C2H2-type 5Disease-causing (★)

Diseases related to Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities

Frequently asked questions

Which genes are linked to Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities?

In CATVariant, Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities is linked to 1 analyzed protein: BCL11B (B-cell lymphoma/leukemia 11B).

How many genetic variants are linked to Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities?

31 variants: 3 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 19 are of uncertain significance or have conflicting reports.

Which uncertain variants in Intellectual developmental disorder with speech delay, dysmorphic facies, and t-cell abnormalities 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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