Notably, compound II enhanced Bax/Bcl-2 ratio and the level of active-caspase 3, indicating that compound II inhibited HCC, at least partly, through mediating caspase-3-dependent apoptosis, as evidenced by Western blot, caspase 3 inhibitor, and caspase 3 siRNA. This evidence concerns the gene BCL2 and hepatocellular carcinoma.