In the normal kidney, ligand binding to MET mediates the activation of the MAPK, STAT, and a variety of other signaling pathways and promotes increased cell growth, scattering and motility, invasion, protection from apoptosis, branching morphogenesis, and angiogenesis [40]. MET overexpression in transgenic mice led to spontaneous development of hepatocellular carcinoma and and inactivation of the MET gene to tumor regression [41]. Here, MET is linked to hepatocellular carcinoma.