Cystic adventitial disease (CAD) is a very rare vascular disorder with prevalence as low as 1:1000 of all vascular pathologies (1). This disease most frequently occurs in young or middle-aged male patients with male/female ratio of 5/1 (1). CAD causes cystic degeneration of peripheral arteries; however, rarely, veins can also be involved (2). Although the most frequently detected location of CAD is the popliteal artery (usually unilateral), any peripheral artery adjacent to the joint can be affected (3). As a result, luminal narrowing or even occlusion may develop due to external compression presenting clinically as intermittent claudication. Pathologic findings of CAD include intramural cysts containing gelatinous material located between the media and the adventitia. Histopathologic examinations report contents of fibrinogen, hyaluronic acid, hydroxyproline, or mucin within the cyst (3). The etiology of CAD is unclear. Several hypotheses including developmental, ganglionic, microtraumatic and degenerative causes have been proposed (4). The developmental hypothesis (the most widely accepted) suggests that the adventitia of affected arteries contains undifferentiated mesenchymal cells, which do not migrate to the joints and secretes mucoid material into the vessel wall. The ganglion hypothesis proposes that adventitial cysts are composed of ectopic synovial ganglions, which migrated from the adjacent joint capsule into the adventitia. The microtraumatic theory suggests that continuous movement of adjacent joints