These include MET gene amplification and increased constitutive phosphorylation of the receptor following exposure to the MET inhibitor PHA-665752 in “MET-driven” gastric cancer cells [59], as well as compensatory EGFR/MET crosstalk, which has been implicated in tumorigenesis and resistance to MET inhibition in colorectal cancer and hepatocellular carcinomas (HCCs) [60,61]. This evidence concerns the gene MET and hepatocellular carcinoma.