The phenomenon of ischemic conditioning as a form of cardioprotection against ischemia was described by Murry et al in 1986 as activation of endogenous cardioprotective mechanisms to limit myocardial infarct size through repeated cycles of nonlethal ischemia‐reperfusion before an index episode of prolonged ischemic injury.30 Ischemic conditioning exerts its cardioprotective effects via ligands such as adenosine, bradykinin, and opioid cell surface receptors acting on downstream signaling cascades involving recruitment of what has been termed the reperfusion injury salvage kinase pathway. This evidence concerns the gene KNG1 and myocardial infarction.