RUNX1 and myocardial infarction: This discrepancy is not surprising given that although Runx1 expression is reported in neonatal cardiomyocytes, it decreases to minimal levels in adult cardiomyocytes.5,6 However, studies have demonstrated that Runx1 is reactivated in cardiomyocytes of the border zone (BZ) region adjacent to the infarct in both patients with MI and experimental animal models.5,7 Whether activation of Runx1 in adult cardiomyocytes after MI is simply a marker of myocardial damage or actually plays a role in the progression of adverse cardiac remodeling is currently unknown.