Cardiomyocyte injury can result from numerous factors, including endotoxin-induced inflammation, myocardial infarction (MI), ischemia/reperfusion (I/R), and doxorubicin (Dox) administration.440 In LPS and Nigerian bacteriocin-stimulated cardiomyocytes, Yu et al. suggested that GSDMD-NT translocated from mitochondria to cytoplasmic membranes in a time-dependent manner.56 In mitochondria, GSDMD-NT is capable of binding to LC3B, and GSDMD-induced mitochondrial damage results in inhibition of autophagic fluxes. Here, MAP1LC3B is linked to myocardial infarction.