For example, CD4 + T cells promoted myocardial ischemia–reperfusion injury through IFN-γ expression (59); CD8 + T cells induced by cytomegalovirus (CMV) infection participated in acute coronary events (60, 61); macrophage Smad3 signaling stimulated phagocytosis and regulated inflammation, which protected the infarction heart, reduced mortality (62); chemokines, such as CCL2 and CXCL12, were involved in cardiac injury, repaired and remodeled by dominating the inflammatory cascade (63, 64). This evidence concerns the gene CD8A and cytomegalovirus infection.