Carnitine acylcarnitine translocase deficiency: genes and variants

Carnitine acylcarnitine translocase deficiency is linked to 1 analyzed protein (SLC25A20). 9 DNA variants are known to cause it; 63 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: carnitine-acylcarnitine translocase deficiency

Genes linked to Carnitine acylcarnitine translocase deficiency

Where Carnitine acylcarnitine translocase deficiency variants cluster

Known disease-causing variants in Carnitine acylcarnitine translocase deficiency

VariantPositionProtein partClinical label
SLC25A20 D231H231Solcar 3Disease-causing (★★)
SLC25A20 R133W133Solcar 2Disease-causing (★★)
SLC25A20 R275Q275Solcar 3Disease-causing (★★)
SLC25A20 A281V281Solcar 3Disease-causing (★★)
SLC25A20 R178Q178Solcar 2Disease-causing (★★)
SLC25A20 Q238R238Solcar 3Disease-causing (★★)
SLC25A20 G81R81Solcar 1Disease-causing (★)
SLC25A20 P230R230Solcar 3Disease-causing (★)
SLC25A20 M1V1Disease-causing (★)

Frequently asked questions

Which genes are linked to Carnitine acylcarnitine translocase deficiency?

In CATVariant, Carnitine acylcarnitine translocase deficiency is linked to 1 analyzed protein: SLC25A20 (Mitochondrial carnitine/acylcarnitine carrier protein).

How many genetic variants are linked to Carnitine acylcarnitine translocase deficiency?

93 variants: 9 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 63 are of uncertain significance or have conflicting reports.

Which uncertain variants in Carnitine acylcarnitine translocase deficiency 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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