Taken together, these data suggest that garcinol, being able to inhibit phosphorylation and acetylation of STAT3, can impair its nuclear localization and DNA binding ability, thereby negatively regulate transcriptional activation ability of STAT3 and ultimately lead to reduced proliferation as well as induction of apoptosis in HCC; therefore, could be exploited as a potential antineoplastic therapeutic in HCC. This evidence concerns the gene STAT3 and hepatocellular carcinoma.