The link between these conditions may be due to the fact that atherosclerosis is a chronic inflammatory disease of the endothelium, characterized by infiltration, deposition of deposits and lipid oxidation, stimulating a self-perpetuating inflammatory state.[8,58] In atherosclerosis, the inflammatory signaling pathways toll-like receptor 4/nuclear factor kappa β and JAK/STAT are activated, which exacerbates inflammation, leading to increased cytokine production and subsequent activation of immune cells. The gene discussed is TLR4; the disease is atherosclerosis.