When the constitutively active EGF receptor variant, EGFRvIII, is targeted with tyrosine kinase inhibitors in glioblastoma, increased expression of uPA is observed; the uPA binds to uPAR, activating uPAR-dependent cell signaling, which promotes cell survival in the absence of functional EGFRvIII (29, 60). This evidence concerns the gene PLAUR and glioblastoma.