As the ATM/mTOR signaling, Rac1-GTPase, and PI3 K/AKT pathways play critical roles in controlling migration of cell [1–4], the multiple cell surface antigens such as CCR2/CD192, CD64/FcγR1, CX3CR1 and Mac3 were linked to origination of monocyte-macrophage differentiation and polarization in post myocardial infarction (MI) [5–9], but the molecular basis of macrophages migrating into specific tissues under physiological or pathological conditions, and fundamental knowledge of cell–cell recognition are much more obscure. Here, RAC1 is linked to myocardial infarction.