The proto-oncogene Met (c-Met, HGF/SF Receptor, HGFR) is a receptor tyrosine kinase that is activated upon Hepatocyte Growth Factor (HGF) binding. This stimulates the autophosphorylation on Tyr1234/Tyr1235 which leads to pleiotropic downstream signaling events in epithelial cells that stimulate multiple cellular processes including cell proliferation, growth, differentiation, cell migration/ invasion, and tumorigenesis. These effects are mediated by SH2 domain-containing proteins that bind to the C-terminal tail of c-Met. Chronic stimulation of Met on cancer cells is thought to play a role in metastasis and dysregulation of c-Met activity is directly associated with oncogenesis, making it an important cancer target.