EGFR and glioblastoma: Unlike TKIs, the immunotoxins rE/CUS, like D2C7-(scdsFv)-PE38KDEL which can be activated in glioblastoma patients expressing wild-type EGFR only or co-expressing wild-type EGFR and EGFRvIII [55], is solely depends on the expression of EGFR rather than tyrosine kinase signaling cascade triggered by EGFR.