Recent experimental results have shown that the c-Met receptor and c-Met-dependent signalling can be specifically inhibited (Christensen et al, 2005), similar to therapies targeting other molecules with, for example, mutant c-Kit in gastrointestinal stromal tumours, trastuzumab in breast cancers overexpressing HER-2, bevacizumab in colorectal carcinoma and genitinib in non-small-cell lung cancer (Birchmeier et al, 2003; Christensen et al, 2005). The gene discussed is MET; the disease is breast carcinoma.