It is believed that miR-155 not only promotes chronic inflammation by enhancing T cell development via the downregulation of cytotoxic T-lymphocyte associated protein 4 (CTLA4), but also blocks mothers against decapentaplegic homolog (SMAD2) translation and protein synthesis during the regulation of TGF-β signaling, leading to AAA development. Here, TGFB1 is linked to triple-A syndrome.