Specifically, we identified TIMP1, APOD and NAD+, among others, to have been highly propagated.39, 40, 41 It is known that TIMP1 inhibits metalloproteinases and it was shown to directly mediate protection from I/R injury in a rat model of myocardial infarction.39 Other genes, such as BCLA1, MT2, Saa3 and Usp17la, have likewise been demonstrated to exercise positive influences on cell survival.42, 43, 44, 45, 46. The gene discussed is APOD; the disease is myocardial infarction.