Indeed, genetic deletion of Siah2 prevented AKAP121 degradation after coronary artery ligation, and this effect was associated with reduced infarct size and enhanced survival after MI in Siah2-/- mice compared to wt. These results suggest that modulation of AKAP121 levels by Siah2 during myocardial ischemia might be crucial for cardiomyocyte survival and, in turn, for post-ischemic cardiac remodeling and survival. Here, AKAP1 is linked to myocardial infarction.