Mechanisms resulting in constitutive or prolonged activation of c‐MET during tumor growth or cancer progression include the occurrence of specific genetic lesions, including translocations, gene amplifications and activating mutations; and transcriptional upregulation of the c‐MET protein in the absence of gene amplification or via ligand‐dependent autocrine or paracrine mechanisms (Danilkovitch‐Miagkova and Zbar, 2002). Here, MET is linked to neoplasm.