Inflammation has been considered a key pathological feature in Ang II‐induced AAA, characterized by enhanced inflammatory infiltration and release of pro‐inflammatory cytokines.29, 30 Previous studies reported that NONO may play a part in the cAMP‐signalling cascade to control its downstream inflammatory genes.12, 31 In this study, NONO silencing significantly reduced the accumulation of macrophages in AAA tissues and markedly reduced the manifestation levels of pro‐inflammatory cytokines, comprising MCP‐1, IL‐6, IL‐1β as well as TNF‐α. The gene discussed is TNF; the disease is triple-A syndrome.