For more than a decade, the role of angiogenesis and vascular endothelial growth factor (VEGF) in relation to tumor growth has been the object of intense research. From 1939 onwards, it was postulated that “the rapid growth of tumor transplants is dependent upon the development of a rich vascular supply” (1,2). Soluble, diffusible factors were held responsible for this new vessel formation (3,4). In 1971, Folkman proposed that antiangiogenesis might be an effective strategy to treat human cancers (5). The identification of VEGF as a potent, diffusible factor affecting vascular endothelial cells led to ongoing investigations focused on VEGF (also referred to as VEGFA) as a key molecule in physiological and pathological vessel formation (6,7). Despite the knowledge that most of the steps in tumor growth are highly complex and multifactorial processes, VEGFA has been shown to be a prerequisite in tumor growth.