The probable reasons for these findings are as follows: (1) LRG1 induces a series of biological processes, including inflammatory response, Th17 differentiation, and endothelial dysfunction, to facilitate atherosclerotic progression and increase the risk of plaque rupture, which further results in a worse prognosis in patients with STEMI (13, 32). This evidence concerns the gene LRG1 and endothelial dysfunction.