RUNX1 and myocardial infarction: At 2 weeks following myocardial infarction, cardiomyocytes isolated from Runx1-deficient hearts had an increased amplitude of sarcoplasmic reticulum (SR)-mediated Ca2+ release stimulated electrically, a faster removal rate of calcium from the cytosol by the SR Ca2+-ATPase (SERCA) and a higher SR content [5].