In summary, we have determined that cetuximab-IONPs bind to both the wtEGFR and the EGFRvIII deletion mutant on human patient-derived GBM cells (including GSCs), inhibit EGFR cell signaling, are internalized by the tumor cells, and promote internalization of the EGFR resulting in enhanced apoptosis. The gene discussed is EGFR; the disease is glioblastoma.