Jghef et al. confirmed that excessive release of proinflammatory cytokines, including IL-6, IL-1β, TGF-β1 and TNF-α, can occur in ISO-induced acute myocardial infarction, myocardial fibrosis and heart failure; among these cytokines, IL-1β is the most critical inflammatory mediator, causing neutrophils and macrophages to accumulate in the damaged myocardium, further promoting the release of more inflammatory cytokines and aggravating myocardial inflammatory injury [28–30]. This evidence concerns the gene IL1B and acute myocardial infarction.