Furthermore, rapamycin, a classic autophagy inducer, was also reported to contribute to the attenuation of cardiac remodeling and dysfunction after acute myocardial infarction through the suppression of the overactivated NF-κB-mediated inflammatory cascade, since the occurrence of acute myocardial infarction was reported to contribute to the overwhelming induction of inflammatory reaction (Wu et al., 2014). Here, NFKB1 is linked to acute myocardial infarction.