On the other hand, activated ERK1/2 and its downstream effectors were strongly upregulated in the miscroscopic, residual lesions in the livers of Akt/Ras mice [13], thus indicating the potential existence of a functional crosstalk between PI3K/Akt and Ras/Raf/MEK/ERK1/2 pathways along hepatocarcinogenesis, whose inhibition might be highly beneficial for the treatment of HCC patients. This evidence concerns the gene RAF1 and hepatocellular carcinoma.