CCL2 and triple-A syndrome: Hyperhomocysteinemia (HHcy) promoted Ang II‐induced AAA information, it is showed that proinflammatory IL‐6 and MCP‐1 were colocalized with AF in HHcy and Ang II mice, Hcy sequentially stimulated AF transformation into myofibroblasts, confirmed the essential role of AF in AAA; cylindromatosis (CYLD) also aggravated CaPO4‐induced AAA by inducing AF activation (secret proinflammatory cytokines) and transformation.11