In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators.

This protein is activated by, and mediates the responses of many cell ligands, such as IL2, IL3, IL7 GM-CSF, erythropoietin, thrombopoietin, and different growth hormones.

Activation of this protein in myeloma and lymphoma associated with a TEL/JAK2 gene fusion is independent of cell stimulus and has been shown to be essential for the tumorigenesis.

[11] Many studies have indicated a key role of STAT5a in leukemia, breast, colon, head and neck, and prostate cancer.

[11][14] STAT5a is involved in the maintenance of integrated prostate epithelial structure and has been shown to be critical for cell viability and tumor growth.

Studies originally showed a correlation between high STAT5a expression and tumor differentiation in mice models, but histopathological analysis of human breast cancer tissue has shown a different trend.