Our results confirmed the role of miR-29 in fibrosis through its targets COL1A1/COL1A234 .We also found miR-29 could inhibit MCL1 in the subnetwork, which is consistent with reports that antagomirs against miR-29 increased Mcl-1 expression and significantly reduced myocardial infarction size35. The gene discussed is MCL1; the disease is myocardial infarction.