Moreover, we demonstrated an additional layer of regulation by FAK of EZH2, since FAK depletion reduced HCC growth in vitro and in vivo by preventing the expression of EZH2 and other cancer-promoting genes, through the reduction of the binding of the TFs E2F2/3 to the EZH2 promoter, thus causing a consequent decrease of H3K27me3 levels [29]. This evidence concerns the gene EZH2 and hepatocellular carcinoma.