Familial hypobetalipoproteinemia 1: genes and variants

Familial hypobetalipoproteinemia 1 is linked to 2 analyzed proteins (APOB and ANGPTL3). 8 DNA variants are known to cause it; 1,250 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 hypobetalipoproteinemia 2

Genes linked to Familial hypobetalipoproteinemia 1

Known disease-causing variants in Familial hypobetalipoproteinemia 1

VariantPositionProtein partClinical label
APOB R3527W3527Disease-causing (★★)
APOB R490W490VitellogeninDisease-causing (★★)
APOB K3394T3394Basic (possible receptor binding region)Disease-causing (★)
APOB R3527L3527Disease-causing (★)
APOB K3394N3394Basic (possible receptor binding region)Disease-causing (★)
ANGPTL3 F295L295Fibrinogen C-terminalDisease-causing
APOB S1524F1524Disease-causing
APOB V352F352VitellogeninDisease-causing

Which prediction tools work for Familial hypobetalipoproteinemia 1

How often each tool ranks a disease-causing variant above a harmless one (AUROC × 100).

Diseases related to Familial hypobetalipoproteinemia 1

Frequently asked questions

Which genes are linked to Familial hypobetalipoproteinemia 1?

In CATVariant, Familial hypobetalipoproteinemia 1 is linked to 2 analyzed proteins: APOB (Apolipoprotein B-100) and ANGPTL3 (Angiopoietin-related protein 3).

How many genetic variants are linked to Familial hypobetalipoproteinemia 1?

1,576 variants: 8 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 1,250 are of uncertain significance or have conflicting reports.

Which uncertain variants in Familial hypobetalipoproteinemia 1 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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