Furthermore, in a mouse myocardial infarction (MI) model, SESN2 was elevated in cardiac macrophages and had a negative regulatory effect on the pro-inflammatory response of M1 macrophages via inhibiting TNF-α, IL-6, and IL-1β expression, thereby polarizing to the M2 phenotype and alleviating excessive inflammation. This evidence concerns the gene IL6 and myocardial infarction.