Because AXL and MET have been shown to become transactivated by RTK heterodimerization with EGFR and EGFRvIII [23,24] and to initiate compensatory signaling pathways in the context of resistance to EGFR inhibitors in several cancers, including GBM [25,26,27,28], we assessed the potential contribution of these RTKs to STAT5 phosphorylation. This evidence concerns the gene EGFR and glioblastoma.