At present, it is generally believed that unlike NSCLC, mutations in TKIs (such as sorafenib) targets, which include receptor tyrosine kinases (RTKs, such as vascular endothelial growth factor receptor [VEGFR], platelet-derived growth factor [PDGFR], or c-kit or the kinase associated with the mitogen-activated protein kinase/phosphoinositide 3 kinase protein kinase B [MAPK/PI3K-AKT pathway]) in HCC cells are not the main mechanism for the difference in sensitivity or resistance to sorafenib in HCC patients [37, 38]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.