In human carcinomas, the receptor tyrosin kinase c-Met becomes activated through several mechanisms, including (i) overexpression and constitutive kinase activation in the presence or absence gene amplification, (ii) paracrine and autocrine activation, (iii) upregulation by mutation or epigenetic mechanisms such as secreted growth factors, tumour hypoxia and activation of other oncogenes (Birchmeier et al, 2003; Pennacchietti et al, 2003; Christensen et al, 2005). The gene discussed is MET; the disease is neoplasm.