It has been assumed that several underlying molecular mechanisms are stimulated after the injection of EPCs into ischemic tissues.92 For example, EPCs are capable of ensuring cardiac tissue regeneration via the reduction of oxidative stress.93 Xue et al found that moderate-to-high doses of EPCs blunt the oxidative stress (8-iso-prostaglandin F2α↓, and SOD↑), and endoplasmic reticulum stress (GRP78 and CHOP) in a rat model of acute MI.94 Of course, prolonged exposure to insulting conditions contributes to the induction of oxidative stress in EPCs. Here, DDIT3 is linked to myocardial infarction.