Studies have shown that in non-reperfusion MI, limiting the expression and infiltration of monocytes/macrophages in the infarcted myocardium and reducing the expression of inflammatory cytokines such as IL-1β, IL-6, IL-17 and TNF-α produced by M1 macrophages play a decisive role in regulating ventricular remodeling and the extent of myocardial necrosis (Henning et al., 2008). Here, IL1B is linked to myocardial infarction.