In an endothelial inflammation model, Klf2 upregulation inhibited the NLRP3/Caspase‐1/IL‐1β pathway, reducing inflammation.[57] It also mediated the expression of Forkhead Box Protein P1 in atherosclerosis‐prone endothelial cells induced by simvastatin, attenuating NLRP3 inflammasome activation and vascular inflammation.[58] Additionally, Klf2 inhibited oxidized LDL‐induced NLRP3 inflammasome activation and endothelial cell pyroptosis.[59] In this study, exercise significantly increased Klf2 expression in microglia/macrophages, an effect reversed by circFndc3b knockdown. This evidence concerns the gene KLF2 and inflammatory response.