In HCC, hyperactive Akt signaling inhibits FOXO1 transcriptional activity, weakens defense against oxidative stress, and as FOXO1 normally suppresses the expression of epithelial mesenchymal transition (EMT)-inducing transcription factors and transforming growth factor-β (TGF-β), leads to subsequent EMT and increased HCC cell migration and invasion [57]. This evidence concerns the gene TGFB1 and hepatocellular carcinoma.