Recently, evidence obtained from vascular inflammation models strongly supports the hypothesis that TMAO can induce inflammation and immune regulation by directly inducing the expression of TNFα, NLRP3 inflammasome, mitochondrial ROS, and NF-κB, which are critical pro-inflammatory mediators, and down-regulating anti-inflammatory cytokines, such as IL-10 [172,173]. The gene discussed is NFKB1; the disease is inflammation.