Both cathepsin B and urokinase-type plasminogen-activated receptor (uPAR) are overexpressed in tumor angiogenesis, and their inhibition can inhibit tumor cell–induced endothelial cell migration by disrupting the JAK/STAT pathway, synthesis of VEGF receptor-2, cyclin D1 and cyclin-dependent kinase, inhibits tumor angiogenesis (124). This evidence concerns the gene SOAT1 and neoplasm.