However, due to the intratumor heterogeneity of HCC (23), the malignant transformation of liver cannot be fully explained by alternations in one or several particular signaling molecules (e.g., KRAS, BRAF, MEK, and ERK) and/or oncogenic pathways (e.g., AKT/mTOR, MAPK, and Wnt/β-catenin). This evidence concerns the gene KRAS and hepatocellular carcinoma.