The level of improved contractility was equivalent to that observed in cardiomyocyte-specific Runx1-deficient mice.21 One unexpected difference between the two approaches was that, in contrast to direct BZ myocardial injection of Ad-Runx1-shRNA, intravenous injection of AAV9-Runx1-shRNA produced a reduction in infarct size following MI. The gene discussed is RUNX1; the disease is myocardial infarction.