# NFKBIA

Source: https://onco.cc/targets/nfkbia/  
OnCo record `nfkbia` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

NFKBIA (NF-kappa-B inhibitor alpha) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Multiple myeloma and Diffuse large B-cell lymphoma.

## Summary

Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL (RELA/p65 and NFKB1/p50) dimers in the cytoplasm by masking their nuclear localisation signals. On cellular stimulation by immune and pro-inflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription.

CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. IntOGen calls it a driver in 5 cohorts (0 activating, 5 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS, Malignant Lymphoma, Non-Hodgkin Lymphoma, Plasma Cell Myeloma.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: NFKB inhibitor alpha; NF-kappa-B inhibitor alpha; MAD-3; IkappaBalpha; NFKBI
- Tags: cancer-genes-wave
- Symbol: NFKBIA
- Class: tumor-suppressor
- Biology: Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL (RELA/p65 and NFKB1/p50) dimers in the cytoplasm by masking their nuclear localisation signals. On cellular stimulation by immune and pro-inflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription. Location: Cytoplasm; Nucleus (UniProt). Locus 14q13.2 (HGNC).
- Where found: Non-Hodgkin lymphoma: IntOGen driver in 2 cohorts (MLYM, NHL); Multiple myeloma: IntOGen driver in 1 cohort (PCM); Diffuse large B-cell lymphoma: CIViC evidence names this disease; IntOGen driver in 2 cohorts (DLBCLNOS)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 5 cohorts; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:7797: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:7797
- UniProt P25963: https://www.uniprot.org/uniprotkb/P25963/entry
- NCBI Gene 4792: https://www.ncbi.nlm.nih.gov/gene/4792
- Ensembl ENSG00000100906: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000100906

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/)
- cancers: [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Multiple myeloma](https://onco.cc/cancers/multiple-myeloma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/)

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JSON: https://onco.cc/api/v1/entities/nfkbia.json