Spautin-1 treatment aggravated myocardial fibrosis by increasing collagen deposition and upregulated the expression of the fibrotic markers including MMP9, collagen type I, and α-SMA, or promoted myocardial apoptosis and increased serum LDH levels, which neutralized the protective effect of FSTL1 in T2DM mice that underwent MI surgery. The gene discussed is MMP9; the disease is myocardial infarction.