Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections: genes and variants

Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections is linked to 2 analyzed proteins (STAT6 and STAT3). 6 DNA variants are known to cause it; 0 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 Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections

Known disease-causing variants in Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections

VariantPositionProtein partClinical label
STAT6 D419H419Disease-causing (★)
STAT6 D419Y419Disease-causing
STAT6 D419G419Disease-causing
STAT6 E372K372Disease-causing
STAT6 E382Q382Disease-causing
STAT6 D519H519SH2Disease-causing

Diseases related to Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections

Frequently asked questions

Which genes are linked to Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections?

In CATVariant, Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections is linked to 2 analyzed proteins: STAT6 (Signal transducer and activator of transcription 6) and STAT3 (Signal transducer and activator of transcription 3).

How many genetic variants are linked to Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections?

12 variants: 6 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 0 are of uncertain significance or have conflicting reports.

Which uncertain variants in Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections 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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