Lother Hennighausen, et al. find CCl4 induces liver tumorigenesis in STAT5 knockout mice by increasing TGF-β stability and STAT3 activity, the N-terminal of STAT5 interacts with TGF-β to decrease TGF-β levels, overexpression of N-terminal STAT5 inhibits HCC formation. The gene discussed is STAT3; the disease is hepatocellular carcinoma.