The limited efficacy of molecular therapies targeting EGFR in glioblastomas suggests that the therapeutic efficacy of EGFR inhibition may be circumvented through cross-coupled signaling from other growth factor receptors that are mutated, amplified or overexpressed in these tumors, such as platelet-derived growth factor receptor, alpha polypeptide (PDGFRA), ERBB2 and MET (7). The gene discussed is MET; the disease is glioblastoma.