MET and neoplasm: For example, we have shown that EGFRvIII signaling is amplified through interaction with a range of other receptor tyrosine kinases, especially c-Met.6 Indeed, EGFRvIII forms a heterodimer with c-Met, leading to its direct activation and enhancing its response to the c-Met ligand hepatocyte growth factor.6 As a consequence, the co-targeting of EGFRvIII and c-Met has synergistic anti-tumor activity in mouse xenograft models.6