The observed activation/upregulation of Akt1 [23], Bcl2 and cell survival associated pathways, such as JAK-STAT [24] and NFκB [25]–[28] pathways in both cardiogenin-activated MSCs and EGJ-treated MI hearts propose that EGJ/cardiogenin does have the ability to increase the survival potential of myocytes at risk along infarct rim and MSCs that migrate to the infarct zone. The gene discussed is SOAT1; the disease is myocardial infarction.