We demonstrated that psEVs had the ability to activate the endothelial NLRP3 inflammasome and trigger the subsequent pyroptosis, leading to endothelial dysfunction that is characterized by the disruption of adherens junctions, loss of vascular integrity, increase in vascular permeability, upregulation of adhesion molecules, and accumulation of proinflammatory leukocytes within the growing atherosclerotic plaque [37, 38]. The gene discussed is NLRP3; the disease is endothelial dysfunction.