At present, it is well-established that activation of the EGFR gene via gene amplification and/or mutations, up-regulates the RAS/RAF/MAPK and PI3K signaling pathways, translating into a tumor phenotype consisting of: i) abnormally high cell proliferation and ii) survival of tumor cells, and iii) an increased angiogenesis [11, 42]. This evidence concerns the gene EGFR and neoplasm.