Our finding revealed that myocardial infarct area (44.73 ± 5.25 vs. 0 from Sham), interstitial fibrosis (44.87 ± 1.30 vs. 1.04 ± 0.22 from Sham, P < 0.05) and cardiomyocyte apoptosis (26.01 ± 0.78 vs. 0.48 ± 0.15 from Sham, P < 0.05) were significantly upregulated following 3-day MI, the effect of which was relieved by TBC1D15 overexpression (20.66 ± 2.22 vs. 44.73 ± 5.25 from MI, P < 0.05 for infarct area; 22.69 ± 2.20 vs. 44.87 ± 1.30 from MI, P < 0.05 for interstitial fibrosis; 8.37 ± 1.62 vs. 26.01 ± 0.78 from MI, P < 0.05 for apoptosis) (Figure 1G-L and Figure S2F). The gene discussed is TBC1D15; the disease is myocardial infarction.