Moreover, researchers reported that the presence of ANXA1 can enhance hematopoietic stem/progenitor cell (HSPC) activation, limit excessive monocyte production [63], and result in macrophage polarization [64] to reduce cardiac necrosis, inflammation, hypertrophy, and fibrosis caused by excessive inflammation after myocardial infarction, thereby restoring left ventricular structure and function (Table 4). Here, ANXA1 is linked to myocardial infarction.