It was shown in vitro that deposits of cholesterol and low-density lipoproteins formed during atherosclerosis in the vessel wall interact with toll-like receptors type 4 (TLR4) and activate NLRP3, which leads to an increase in the production of proinflammatory cytokines IL-1β and IL-18 in vitro [110] and in vivo [108,111]. The gene discussed is IL18; the disease is atherosclerosis.