KRAS and neoplasm: Most gene silencing targets are related to oncogenes (e.g., cMYC, KRAS, BCR-ABL, EGFR), which trigger abnormal cell proliferation due to the increase in gene expression or up-activity of the resulting onco-proteins; may also inhibit tumor suppressor genes, that normally prevent cell proliferation and tumor development; or influence other genes related to tumoral survival (e.g., angiogenesis) [29].