We have previously shown that in, U87, T98G and LN443 GBM cells that express wild type EGFR [23], cytostatic concentrations of gefitinib lead to the accumulation of EGFR in enlarged early endosomes and increase EGF endocytosis, a phenomenon we called gefitinib-mediated endocytosis (GME) [22]. This evidence concerns the gene EGFR and glioblastoma.