These conclusions are supported by the following findings: i) c-Met co-localized with CAV1 and this association increased by HGF; ii) HGF induced the activation of c-Met and CAV1; iii) association of activated c-Met with CAV1 resulted in increased migration, invasion and branching morphogenesis; iv) co-existence and colocalization of activated c-Met and CAV1 in HCC tissues (Fig. 11). This evidence concerns the gene CAV1 and hepatocellular carcinoma.