Echocardiography showed that AGGF1 treatment significantly increased LVEF and LVFS, reduced LVEDD, LVESD, cardiac fibrosis, and infarct sizes, and increased LV wall thickness in AAV9-GFP control mice with MI compared with IgG treatment (Fig 8C and 8D), but the therapeutic effect of AGGF1 was completely lost in AAV9-CMV-Cre Atg5 KO mice with deficient autophagy (Fig 8C and 8D). The gene discussed is ATG5; the disease is myocardial infarction.