The differentiation, proliferation and metastasis of kidney cancer are inseparable from the action of many cytokines. The existing targeted therapeutic drugs either act on a single site or on multiple factors, and the commonly used targeted therapeutic drugs for kidney cancer mainly target two aspects: tumor angiogenesis and anti-tumor cell proliferation. Theoretically, the more targets a drug has, the more comprehensive the tumor control will be. Multi-targeted drugs commonly used in clinical treatment of kidney cancer include sorafenib and tinib. Sorafenib is a novel oral multi-kinase inhibitor that strongly inhibits the serine/threonine kinase activity of Raf-1 and inhibits the tyrosine kinase activities of VEGFR-2, VEGFR-3, PDGFR-β, FLT-3 and KIT. Sunitinib is also an orally available small molecule hydroxyindole tyrosine kinase inhibitor that selectively inhibits multiple targets including PDGFR, VEGFR, KIT and FLT3, thereby exerting anti-tumor and anti-angiogenic activities. As targeted therapeutic agents, the adverse effects of sorafenib and sunitinib are very different from those of cytotoxic drugs, often in the form of malaise, skin toxicity, hypertension and diarrhea. Compared to the two drugs, patients taking sorafenib had a lower incidence of adverse reactions such as hypertension, malaise, diarrhea, gastritis, abnormal bleeding and hematologic adverse reactions than patients taking sunitinib, except for skin reactions on hands and feet, rash (or desquamation) and alopecia, which were higher than those of patients taking sunitinib. In addition to the above two multi-targeted drugs, sirolimus mammalian target (mTOR) inhibitor CCI-779, VEGF inhibitor bevacizumab, and single-targeted drugs such as EGFR inhibitors cetuximab, gefitinib and lapatinib have also shown some anti-cancer activity in clinical studies, but their efficacy was not as significant as the above two multi-targeted drugs