Ovarian cancer is characterized by an imbalance between pro- and antiangiogenic factors in favor of angiogenesis activation, with an increase in the tumor levels of proangiogenic factors (i.e., vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factors (PDGFs), tumor necrosis factor (TNF)-alpha, angiopoietins, interleukin (IL-6 and IL-8, etc.)and a decrease in anti-angiogenic factors (i.e., angiostatins, endostatins, etc.)[2]. This evidence concerns the gene VEGFA and neoplasm.