Specifically, in the model of AAA induced by Ang II administration in ApoE−/− mice, RvD2 treatment decreased AAA formation by reducing local pro-inflammatory molecules, including MCP-1, IL-6, IL-1β and RANTES, and MMP2 and MMP9 activity and increased anti-inflammatory cytokines, such as IL-10. This evidence concerns the gene CCL5 and triple-A syndrome.