The depletion of FAK in hepatocytes blocked tumor proliferation and prolonged survival in a c-Met/β-catenin-driven hepatocellular carcinoma (HCC) mouse model (Shang et al., 2015), suggesting that FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis. This evidence concerns the gene PTK2 and hepatocellular carcinoma.