Specifically, PTHrP may act as a preconditioning-mimetic agent (i.e., may limit ischemia-reperfusion-induced cardiomyocyte death and reduce myocardial infarct size) [1], potentially via activation of one or more ‘survival kinases’ that have been identified to contribute to the infarct-sparing effect of ischemic conditioning [14,15,16,17,18,19]. This evidence concerns the gene PTHLH and myocardial infarction.