Plaque rupture is caused by shear stress gradients and activation of Toll-like receptor 2 (TLR-2) in endothelial cells, with subsequent activation and aggregation of neutrophil extracellular traps (NETs) and thrombosis causing a decrease in morbidity outcomes, when compared to plaque rupture as the predominant mechanism, resulting in a non-ST-segment elevation myocardial infarction (NSTEMI) responsible for approximately 40% of patients with acute coronary syndrome (ACS) [30,31]. The gene discussed is TLR2; the disease is acute coronary syndrome.