In this study, using Fn1 inhibitor in an I/R mouse model, we demonstrated that blockage of Fn1 in mice significantly reduced myocardial infarction, cardiomyocyte apoptosis, inflammation, oxidative stress, and fibrosis, leading to improved contractile dysfunction after I/RI (Figures 2, –4), supporting the findings that inhibition of Fn1 improves myocardial I/RI. This evidence concerns the gene FN1 and myocardial infarction.