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The CCRCC, a very highly vascularized tumor, is highly refractory to conventional anti-cancer therapies such as conventional chemotherapies or radiotherapy in locoregional or metastatic forms. Three main molecular pathways (VHL/HIF/VEGF, PI3K/AkT/mTOR and MAP Kinases (Raf/MEK/ERK)) are possibly activated in CCRCC, resulting in a profond disturbance of control of cell growth advantage, metastatic competence, tumor/endothelial cells relationship, and therapy resistance. These molecular pathways have thus been considered to develop novel drugs that have improved clinical outcomes in randomized trials by blocking VEGF receptor or inhibiting mTOR protein. A in vivo tumor model is developed in the laboratory to explore the biological effect of the drugs.