Ebos JM et al. reported in Cancer Cell that using multiple metastasis assays in mice treated for a short period of time, they found that after intravenous injection of tumor cells, or after removal of primary standing growth tumors, the vascular endothelial growth factor receptor (VEGFR) platelet-derived growth factor receptor (VEGFR) kinase inhibitor sunitinib/SU11248 accelerated metastatic tumor growth and reduce overall survival. Accelerated metastasis was also observed in mice treated with sunitinib prior to intravenous implantation of tumor cells, suggesting that there may be “metastatic regulation” in multiple organs. Similar results were observed using additional VEGF receptor tyrosine kinase inhibitors, suggesting a class-specific effect of these drugs. Importantly, in contrast to the accelerated metastasis we observed, a demonstrable antitumor benefit was obtained when the same human breast cancer cells as well as mouse or human melanoma cells grew as primary tumors in normal sites and received the same sunitinib treatment. In combination with several recent publications have found that multikinase targeted therapeutic agents such as sunitinib have a therapeutic effect in primary renal cancer, but that short-term treatment reduces survival in animals with loaded metastases. This suggests that more experimental data are needed on the efficacy of sunitinib in the adjuvant treatment of metastatic kidney cancer, and perhaps the use of these drugs needs to be redesigned. In recent years, multikinase targeted therapy drugs for metastatic kidney cancer have entered the clinic in China. From the experience of our department in treating metastatic kidney cancer, although multikinase targeted therapy is beneficial to patients with metastatic kidney cancer, significant toxic side effects have been observed and the cost is very expensive. Therefore, the drug still has a way to go in terms of clinical effect and expanded application.