In addition, in vitro mechanistic studies indicate that TMAO can induce vascular inflammation and endothelial dysfunction through activating NLRP3 inflammasome and the mitogen-activated protein kinase/nuclear factor-kappa B pathway (Seldin et al., 2016; Boini et al., 2017; Chen et al., 2017), which also plays a critical role in thrombus formation. The gene discussed is NLRP3; the disease is endothelial dysfunction.