Interestingly, as reported for other types of cancers [61], it has been recently demonstrated that GBM therapeutic resistance to EGFR inhibitors may be explained by compensatory activation of EGFR-related family members (ERBB2, ERBB3), and therefore simultaneous shutdown of multiple ERBB family members may be required for more effective GBM therapy [62]. The gene discussed is ERBB3; the disease is glioblastoma.