Apart from activating NF-κB, TMAO also activates NLRP3 inflammasome leading to a proinflammatory milieu that has been demonstrated in human aortic endothelial cells as well as carotid artery endothelial cells implicating TMAO to contribute to endothelial dysfunction and CVD [165,166]. The gene discussed is NLRP3; the disease is endothelial dysfunction.