Th1 cells secrete TNF-α and IFN-γ to promote the further growth of atherosclerotic plaques, while Th17 cells secrete IL17 and IL22, and the release of reactive oxygen species increases, which promotes the formation of new blood vessels and intraplaque hemorrhage; Elevated IL17 levels in plaques may further weaken the fibrous caps in atherosclerotic plaques, leading to plaque rupture and myocardial infarction (1, 7). Here, IL17A is linked to myocardial infarction.