Another report showed that the reduced autophagic responses in OLEFT after myocardial infarction (MI) were associated with a deficiency in AMPK/ULK1 activation, decreased response of AKT/mTOR/S6 signaling, and increased interaction between BECLIN-1 and BCL-2, which are important molecular events for suppressing autophagy. Here, BCL2 is linked to myocardial infarction.