Cardiac and peripheral vascular diseases, ie, atherosclerosis frequently lead to organ dysfunction, death and morbidity. Although some patients may have developed the ability to escape this fatal disorder by bridging the occlusion or stenosis side with “naturally growing bypasses”[1], most patients have to undergo surgical interventions associated with a risk of side effects. For example, cardiopulmonary bypass surgery highly increases the risk for neurological complications and many of the patients undergoing percutaneous transluminal angioplasty suffer from restenosis [2, 3]. Thus, understanding the mechanism of collateral artery growth may generate options for new treatments. These therapies could lead to the enhancement of growth and remodeling processes and therefore assure the recovery of blood flow deficits caused by the arterial disorders. Pioneering work in describing the existence of collateral blood vessels in healthy people as well as in patients undergoing chronic arterial diseases was done by Fulton and Longland [4, 5]. They also found out that in patients with coronary heart diseases these collateral vessels are often enlarged [6]. A body of evidences has been collected since this time showing that the mechanisms leading to the development of large collateral vessels with the capability to efficiently conduct blood obviously differ from the mechanisms usually summarized as angiogenesis. Therefore, the term “arteriogenesis” was established to recognize both, the pivotal differences in both processes, and the fact that the growth of collateral vessels is the most important adaptive process in the vascular system [7]. The reason why only collateral vessels and not capillaries can efficiently compensate flow deficits caused by arterial lesions, can be easily assessed from the law of Hagen-Poiseuille demonstrating that flow (Q) is proportional to the 4th power of vessel diameter (R).