The treatment of human AAA-derived VSMC with Angiotensin II (AngII) results in induction of ASC and the DNA sensor IFI16, whereas overexpression of IFI16 in AngII-treated rat VSMC enhances ROS levels, activates Caspase-1, promotes migration and triggers release of IL-1β [31]. The gene discussed is IFI16; the disease is triple-A syndrome.