MET and hepatocellular carcinoma: Wang et al. (2001) did a trial by using human Met transgenic mice to understand how ligand-independent activation of RTKs affects tumorigenesis. It was found that transgenic mice developed HCC, which subsided when the transgene was inhibited, which showed that Met over-expression induced tumorigenesis without HGF. The HGF/c-Met axis can also induce onset of HCC by promoting angiogenesis (Giordano and Columbano, 2014).