Over the past two decades, alterations within and outside the MET kinase domain have been described in several solid tumours, including NSCLC, glioblastoma, breast, renal and colon cancers, as well as cancers of unknown primary origin, suggesting that activated MET plays a significant role in the tumourigenic process in a wide range of cell types [4,5,6,7,8,9,10,11]. The gene discussed is MET; the disease is glioblastoma.