Despite the inconsistence between different methods used for RUNX1 inhibition which might be due to the general superiority of cardiotropic AAVs, the findings from Martin et al. (Martin et al. 2023) raised the possibility of limiting infarct size post-MI by antagonizing RUNX1 function which requires further validation, particularly at an earlier stage of cardiac damage. This evidence concerns the gene RUNX1 and myocardial infarction.