Apart from showing a strong difference in imbalance between DCM cases and donors, FSTL1 is a known cardioprotective gene, acting as an autocrine/paracrine regulatory factor that antagonizes myocyte hypertrophic growth and the loss of ventricular performance in response to pressure overload [47], and shown to be able to prevent myocardial ischemia/reperfusion injury by inhibiting apoptosis and inflammatory response [48]. This evidence concerns the gene FSTL1 and myocardial ischemia.