Several studies demonstrated the existence of different combinations of abnormal expression and activation of growth factor receptors (such as EGFR, PDGFRα, PDGFRβ, c-kit, met, and ret) in GBM-derived cell lines and primary cultures, suggesting that the co-activation of these receptors may condition the response of GBM cells to targeted therapies [13]. The gene discussed is KIT; the disease is glioblastoma.