Looking at the role of gene pathways that preliminarily raise important expectations, such as EGFR, two main mechanisms have been suggested: target independence, namely, alterations in the target that becomes insensitive to inhibition, and target compensation; in other words, the activation of alternative pathways (96). GBM cells are probably dependent on several growth pathways and are particularly skilled to escape a one-modality attempt. This evidence concerns the gene EGFR and glioblastoma.