Castillero et al. also showed that inhibition of the ActIIR signaling either with decoy myostatin to prevent ligands from binding to ActIIR or with follistatin was associated with preserved cardiac function and fibroblast-driven decrease in cardiac fibrosis in mice following coronary ligation to induce myocardial infarction [63]. This evidence concerns the gene MSTN and myocardial infarction.