RCC represents a prototype of an AA-therapy sensitive tumor due to its unique molecular pathogenesis where inactivation of the Von Hippel–Lindau (VHL) tumor suppressor gene triggers a cascade of pro-angiogenic and thus tumor promoting events, resulting in an increase of growth factors such as VEGF advancing tumor growth, proliferation as well as migration of endothelial cells. The gene discussed is VEGFA; the disease is neoplasm.