In nude mice with xenografted tumors using HAK-1B hepatoma cells, luteolin significantly inhibited the growth of the tumors in a dosage-dependent manner by targetting STAT3 through dual pathways—the ubiquitin-dependent degradation in Tyr705-phosphorylated STAT3 and the gradual downregulation in Ser727-phosphorylated STAT3 through inactivation of CDK5, thereby triggering apoptosis via upregulation in Fas/CD95 (Selvendiran et al. 2006). This evidence concerns the gene STAT3 and hepatocellular carcinoma.