It is worth noting thatrecent studies by Pan et al. [33] have shown that when the autophagyflux is inhibited in the later stage of MI/RI, the activation of TFEB will inducethe accumulation of autophagosomes in cardiomyocytes and promote cellularautophagic death of myocardial cells, which will aggravate myocardial infarctioninjury, while inhibition of endogenous TFEB can alleviate the process of MI/RI.This study indicates that TFEB may be a double-edged sword in MI/RI. This evidence concerns the gene TFEB and myocardial infarction.