Testosterone 17-beta-dehydrogenase deficiency: genes and variants

Testosterone 17-beta-dehydrogenase deficiency is linked to 1 analyzed protein (HSD17B3). 20 DNA variants are known to cause it; 10 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 Testosterone 17-beta-dehydrogenase deficiency

Known disease-causing variants in Testosterone 17-beta-dehydrogenase deficiency

VariantPositionProtein partClinical label
HSD17B3 R80Q80Disease-causing (★★)
HSD17B3 R80W80Disease-causing (★★)
HSD17B3 N130S130Disease-causing (★★)
HSD17B3 E215D215Disease-causing (★★)
HSD17B3 S232L232Disease-causing (★★)
HSD17B3 P282L282Disease-causing (★★)
HSD17B3 A203V203Disease-causing (★★)
HSD17B3 V205E205Disease-causing (★★)
HSD17B3 S65L65Disease-causing (★★)
HSD17B3 N74T74Disease-causing (★★)
HSD17B3 E93K93Disease-causing (★★)
HSD17B3 Q176P176Disease-causing (★★)
HSD17B3 V225M225Disease-causing (★★)
HSD17B3 E214G214Disease-causing (★★)
HSD17B3 A56T56Disease-causing (★)
HSD17B3 M235V235Disease-causing (★)
HSD17B3 M1V1Disease-causing (★)
HSD17B3 C268Y268Disease-causing (★)
HSD17B3 M197K197Disease-causing (★)
HSD17B3 M47V47Disease-causing

Diseases related to Testosterone 17-beta-dehydrogenase deficiency

Frequently asked questions

Which genes are linked to Testosterone 17-beta-dehydrogenase deficiency?

In CATVariant, Testosterone 17-beta-dehydrogenase deficiency is linked to 1 analyzed protein: HSD17B3 (17-beta-hydroxysteroid dehydrogenase type 3).

How many genetic variants are linked to Testosterone 17-beta-dehydrogenase deficiency?

32 variants: 20 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 10 are of uncertain significance or have conflicting reports.

Which uncertain variants in Testosterone 17-beta-dehydrogenase 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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