Genomic DNA aberrations are key genetic events in gliomagenesis. Recurrent genomic regions of alteration, including net gains and losses, have been found in gliomas. Whereas some of these regions contain known oncogenes and tumor suppressor genes, the biologically relevant genes within other regions remain to be identified. The phenotypic and genotypic heterogeneity indicate that no isolated genetic event accounts for gliomagenesis, but rather the cumulative effects of a number of alterations that operate in a concerted manner. In this pathological process are included various biological events, such as activation of growth factor receptor signaling pathways, down-regulation of many apoptotic mechanisms, and imbalance of pro- and antiangiogenic factors. Several growth factor receptors, such epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDRGF), C-Kit, vascular endothelial growth factor receptor (VEGFR) are over-expressed, amplified and/or mutated in gliomas (Figure 2-1). In Table 2-1 are summarized the most common glioma genetic alterations frequently found. In the light of this novel information, the modulation of gene expression at more levels, such as DNA, mRNA, proteins and transduction signal pathways, may represent the most effective modality to down-regulate or silence some specific genic functions or introduce genes, downregulated or deleted selectively, into neoplastic cells.