Persistent activation of STAT3 has been frequently observed in many kinds of tumors [8,9] including HCC [10-12] and this constitutively active STAT3 is thought to contribute to the process of oncogenesis by modulating the expression of various genes required for tumor cell survival (e.g., Bcl-xL, Mcl-1, survivin), proliferation (e.g., cyclin D1, c-Myc), and angiogenesis (e.g., vascular endothelial growth factor [VEGF]) as well as metastasis [8]. This evidence concerns the gene MCL1 and hepatocellular carcinoma.