In this study, we identified that HS had great potential to promote the abundance and translocation of NFAT5, which activates PAI-1-mediated the antifibrinolytic activation and monocytes adhesion/transmigration in ECs, leading to accelerated fibrin deposition and macrophages infiltration in the artery wall, and eventually promoting the development of atherosclerotic lesions. The gene discussed is SERPINE1; the disease is Atherosclerotic lesion.