CCL2 and triple-A syndrome: Sustained inflammation, as represented by upregulation of proinflammatory cytokines (e.g., tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6] and monocyte chemoattractant protein-1 [MCP-1]) and infiltration of inflammatory cells (e.g., macrophages), may play a fundamental role during the initiation and development of AAA.