CCL2 and triple-A syndrome: In AAA, macrophages are recruited prominently to the adventitia and media, where they secrete proteases that lead to matrix degradation, smooth muscle cell apoptosis, tissue weakening, and aortic enlargement.12–13 Macrophage precursor recruitment to the adventitia during AngII‐induced AAA formation was reported to be dependent on adventitial secretion of interleukin‐6 (IL‐6) and monocyte chemotactic protein‐1 (MCP‐1) and of CCR2 expression in monocytes.14 The macrophages accumulating in aortic adventitia were CD14hi and F4/80−, consistent with activated macrophages.