Their mechanisms of action involved direct inhibition of tumor growth by targeting the RAF/MEK/ERK signaling pathway, as well as indirect inhibition of tumor cell proliferation by blocking vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) pathways, which were crucial for tumor neovascularization [66]. The gene discussed is KDR; the disease is neoplasm.