Furthermore, THs disturbances activate the release of inflammatory factors (such as IL-1, IL-2, IL-6, and TNF-α) through oxidative stress (18, 19), and chronic inflammation is a core mechanism of atherosclerosis, promoting plaque instability and thrombus formation, exacerbating myocardial remodeling and ischemia-reperfusion injury. This evidence concerns the gene IL6 and atherosclerosis.