Microvascular complications of diabetes, susceptibility to, 3: genes and variants

Microvascular complications of diabetes, susceptibility to, 3 is linked to 2 analyzed proteins (ACE and HFE). 2 DNA variants are known to cause it; 187 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: Microvascular complications of diabetes, susceptibility to, 4; Microvascular complications of diabetes, susceptibility to, 7

Genes linked to Microvascular complications of diabetes, susceptibility to, 3

Weakly linked (only a few uncertain records): IL1RN.

Known disease-causing variants in Microvascular complications of diabetes, susceptibility to, 3

VariantPositionProtein partClinical label
ACE M1T1Disease-causing (★)
HFE C282Y282Ig-like C1-typeDisease-causing

Same protein, different disease

Diseases related to Microvascular complications of diabetes, susceptibility to, 3

Frequently asked questions

Which genes are linked to Microvascular complications of diabetes, susceptibility to, 3?

In CATVariant, Microvascular complications of diabetes, susceptibility to, 3 is linked to 2 analyzed proteins: ACE (Angiotensin-converting enzyme) and HFE (Hereditary hemochromatosis protein).

How many genetic variants are linked to Microvascular complications of diabetes, susceptibility to, 3?

191 variants: 2 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 187 are of uncertain significance or have conflicting reports.

Which uncertain variants in Microvascular complications of diabetes, susceptibility to, 3 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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