It was shown that the substantial rise in miR–17 expression during a myocardial infarction was connected to significant suppression in the expression of tissue inhibitor of metalloproteinase 1 and 2 (TIMP1/2), which resulted in increased proteolytic matrix metalloproteinase 9 (MMP9) activity and caused an increase in ECM degradation as well as increased post-infarction left ventricular dysfunction [76]. The gene discussed is MMP9; the disease is myocardial infarction.