In this context, GBM treatment with the antineoplastic 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) (carmustine) may induce DNA crosslinks, inhibition of glutathione reductase, and increase of the intracellular oxidative status, events that bring as consequence the pathway activation without c-Cbl phosphorylation and without reductions in EGFR contents (a c-Cbl target frequently overexpressed in GBMs and other cancers) (142, 143). Here, EGFR is linked to glioblastoma.