AKT1 and myocardial infarction: Therefore, it may be a potential therapeutic approach for post-MI cardiac dysfunction.[38] It may also be a promising cardiac regeneration strategy for treating post-MI heart failure.[38] Our results are consistent with previous findings, suggesting that TP53, EGFR, AKT1, STAT3, IL6, IL1B, SRC, and MYC are likely to be the core targets of DSD for the treatment of MI.