# STAT5 (STAT5A, STAT5B)

Source: https://onco.cc/targets/stat5/  
OnCo record `stat5` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

STAT5 is the messenger that carries growth signals from FLT3, JAK2 and BCR::ABL1 into the nucleus and switches on survival genes in leukaemia cells. No drug hits STAT5 directly yet; the FLT3 and ABL inhibitors work by cutting off the signal above it.

## Summary

STAT5A and STAT5B (both on chromosome 17q21.2) are transcription factors with a dual role in signal transduction and transcription: they bind GAS elements and activate prolactin-induced transcription; STAT5A mediates responses to KIT ligand, other growth factors, ERBB4 and possibly activated FGFRs, and STAT5B mediates responses to cytokines, hormones and growth factors including oncostatin M and positively regulates haematopoietic and erythroid differentiation (UniProt P42229, P51692). In OnCo, STAT5 is the downstream node that collapses when gilteritinib, midostaurin and quizartinib block FLT3-ITD and TKD signalling in AML and when ponatinib blocks BCR::ABL1 in Ph-positive leukaemia; the MPL record places it among the proteins docked by the activated thrombopoietin receptor.

## Fields

- Kind: Target
- Last checked: 2026-09-22
- Also known as: STAT5A; STAT5B; signal transducer and activator of transcription 5
- Tags: wave5-target
- Symbol: STAT5A, STAT5B
- Class: transcription
- Biology: The JAK-STAT pathway record lists STAT5 as the STAT of leukaemias, alongside STAT3 as the hub of IL-6-driven survival. Constitutive STAT5 signalling is the readout of FLT3, JAK2, MPL and BCR::ABL1 activity in the corpus mechanism steps, and no direct STAT5 inhibitor is recorded.
- Where found: FLT3-mutant AML (downstream of FLT3-ITD/TKD); Ph-positive CML and ALL (downstream of BCR::ABL1); Myeloproliferative neoplasms (downstream of JAK2 and MPL)

## Notes

- Prevalence not recorded in this wave: HGNC and UniProt carry no positivity rates and no other source was consulted.
- Two genes, so no single HGNC id on the record (the rule in scripts/enrich-target-ids.ts); both are cross-referenced in target-xrefs.ts.

## Sources

- HGNC HGNC:11366 (STAT5A): https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:11366
- HGNC HGNC:11367 (STAT5B): https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:11367
- UniProt P42229 (STAT5A): https://www.uniprot.org/uniprotkb/P42229/entry
- UniProt P51692 (STAT5B): https://www.uniprot.org/uniprotkb/P51692/entry
- NCBI Gene 6776 (STAT5A): https://www.ncbi.nlm.nih.gov/gene/6776
- NCBI Gene 6777 (STAT5B): https://www.ncbi.nlm.nih.gov/gene/6777

## Connected records

- drugs: [Gilteritinib](https://onco.cc/drugs/gilteritinib/), [Midostaurin](https://onco.cc/drugs/midostaurin/), [Ponatinib](https://onco.cc/drugs/ponatinib/), [Quizartinib](https://onco.cc/drugs/quizartinib/)
- targets: [BCR::ABL1 (Philadelphia chromosome)](https://onco.cc/targets/bcr-abl/), [FLT3](https://onco.cc/targets/flt3/), [JAK2](https://onco.cc/targets/jak2/), [MPL (thrombopoietin receptor)](https://onco.cc/targets/mpl/)
- cancers: [Acute lymphoblastic leukaemia](https://onco.cc/cancers/all-leukemia/), [Acute myeloid leukaemia](https://onco.cc/cancers/aml/), [Chronic myeloid leukaemia, accelerated and blast phase](https://onco.cc/cancers/cml-advanced-phase/), [FLT3-mutated acute myeloid leukaemia](https://onco.cc/cancers/aml-flt3/)
- pathways: [Acute myeloid leukaemia (KEGG map)](https://onco.cc/pathways/aml-signalling/), [BCR::ABL1 (Philadelphia chromosome)](https://onco.cc/pathways/bcr-abl1-signalling/), [Chronic myeloid leukaemia (KEGG map)](https://onco.cc/pathways/cml-signalling/), [JAK-STAT signalling](https://onco.cc/pathways/jak-stat/)

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JSON: https://onco.cc/api/v1/entities/stat5.json