Considering the documented atheroprotective function of IDO1 in established atherosclerosis, we hypothesized that high IDO1 and TDO expression and/or activity might be a self-protective mechanism for atherosclerosis in advanced stages and that the comparable downregulation of IDO1 and TDO in advanced atherosclerosis led to post-myocardial infarction. Here, TDO2 is linked to myocardial infarction.