Studies have proven that TMAO plays a role in the atherosclerosis process through mediating immune response by recruiting macrophages to aortic lesions with increased CD36, tumor necrotic factor α, and interleukin-6 expressions through the p38 MAPK and JNK 1/2 pathways [37], or activation of NLRP3 inflammasome to cause endothelial dysfunction and inflammation through redox regulation and lysosomal dysfunction [38]. The gene discussed is NLRP3; the disease is endothelial dysfunction.