Familial hemophagocytic lymphohistiocytosis: genes and variants

Familial hemophagocytic lymphohistiocytosis is linked to 4 analyzed proteins (UNC13D, CDC42, SLC2A10 and COL3A1). 8 DNA variants are known to cause it; 449 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Also known as: Familial hemophagocytic lymphohistiocytosis 3; familial hemophagocytic lymphohistiocytosis type 1

Genes linked to Familial hemophagocytic lymphohistiocytosis

Weakly linked (only a few uncertain records): ACTA2, TGFBR1, FHL1, MYH11 and TGFB2.

Where Familial hemophagocytic lymphohistiocytosis variants cluster

Known disease-causing variants in Familial hemophagocytic lymphohistiocytosis

VariantPositionProtein partClinical label
UNC13D R414C414Interaction with RAB27ADisease-causing (★★)
UNC13D R414L414Interaction with RAB27ADisease-causing (★★)
UNC13D A1018D1018C2 2Disease-causing (★★)
CDC42 R186C186Disease-causing (★★)
UNC13D E616G616MHD1Disease-causing (★★)
UNC13D L1058P1058Disease-causing (★)
UNC13D L403P403Interaction with RAB27ADisease-causing (★)
UNC13D F857C857MHD2Disease-causing

Same protein, different disease

Diseases related to Familial hemophagocytic lymphohistiocytosis

Frequently asked questions

Which genes are linked to Familial hemophagocytic lymphohistiocytosis?

In CATVariant, Familial hemophagocytic lymphohistiocytosis is linked to 4 analyzed proteins: UNC13D (Protein unc-13 homolog D), CDC42 (Cell division control protein 42 homolog), SLC2A10 (Solute carrier family 2, facilitated glucose transporter member 10) and COL3A1 (Collagen alpha-1(III) chain).

How many genetic variants are linked to Familial hemophagocytic lymphohistiocytosis?

528 variants: 8 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 449 are of uncertain significance or have conflicting reports.

Which uncertain variants in Familial hemophagocytic lymphohistiocytosis 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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