Upregulation of endogenous alternatively spliced tumourigenic variants is frequently observed in many cancers such as the proangiogenic splice variant of vascular endothelial growth factor (VEGF165), an epithelial-mesenchymal transition-inducing isoform of Rac1 (Rac1b), and the cancer-initiating form of protein kinase C (PKCβII) [10,11,12,13]. This evidence concerns the gene VEGFA and cancer.