Sorafenib exerts its therapeutic effects by inhibiting the extracellular-signal-regulated kinase (ERK)-independent activities of Raf1, thereby causing tumor cell apoptosis, and suppressing the activity of receptor tyrosine kinases (RTKs) such as vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, as well as platelet-derived growth factor receptor beta (PDGFR-β), thereby inhibiting tumor angiogenesis and promoting apoptosis (23, 34, 35). The gene discussed is RAF1; the disease is neoplasm.