Borjeson-Forssman-Lehmann syndrome: genes and variants

Borjeson-Forssman-Lehmann syndrome is linked to 1 analyzed protein (PHF6). 12 DNA variants are known to cause it; 35 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 Borjeson-Forssman-Lehmann syndrome

Where Borjeson-Forssman-Lehmann syndrome variants cluster

Known disease-causing variants in Borjeson-Forssman-Lehmann syndrome

VariantPositionProtein partClinical label
PHF6 C45Y45C2HC pre-PHD-type 1Disease-causing (★★)
PHF6 M1T1Disease-causing (★★)
PHF6 E139D139Disease-causing (★)
PHF6 V268L268Extended PHD2 domain (ePHD2)Disease-causing (★)
PHF6 A140T140Disease-causing (★)
PHF6 H229R229C2HC pre-PHD-type 2Disease-causing
PHF6 G248V248C2HC pre-PHD-type 2Disease-causing
PHF6 C305F305PHD-type 2Disease-causing
PHF6 C99F99PHD-type 1Disease-causing
PHF6 K234E234C2HC pre-PHD-type 2Disease-causing
PHF6 S49L49C2HC pre-PHD-type 1Disease-causing
PHF6 C297F297PHD-type 2Disease-causing

Diseases related to Borjeson-Forssman-Lehmann syndrome

Frequently asked questions

Which genes are linked to Borjeson-Forssman-Lehmann syndrome?

In CATVariant, Borjeson-Forssman-Lehmann syndrome is linked to 1 analyzed protein: PHF6 (PHD finger protein 6).

How many genetic variants are linked to Borjeson-Forssman-Lehmann syndrome?

63 variants: 12 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 35 are of uncertain significance or have conflicting reports.

Which uncertain variants in Borjeson-Forssman-Lehmann syndrome 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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