INS and myocardial infarction: DNA damaging-induced transcript 4 (DDIT4) is induced by various cellular stress conditions, such as hypoxia, endoplasmic reticulum stress and oxidative stress.[27] DDIT4 can inhibit the activity of rapamycin complex 1 (mTORC1), which is a major participant in cell growth, proliferation and survival, and thus regulate cell apoptosis.[28] Importantly, DDIT4 has been shown to promote apoptosis and autophagy in myocardial infarction,[29] insulin reperfusion,[30] ataxia telangiectasia.[31] This provides a greater possibility for DDIT4 to participate in the evolution of ruptured AAA.