Signals induced by lipopolysaccharide (LPS) [55] can activate pro-IL-18 and pro-IL-1β to activated IL-18 and IL-1β via NF-κB, which can then activate liver fibrosis via proinflammatory cytokines, or they can act directly on NLRP3 inflammatory vesicles, which in turn activate its downstream signaling pathway caspase-1 via NLRP3 inflammasomes which in turn will promote proinflammatory processes in the maturation and secretion of the precursors pro-IL-1β and pro-IL-18 during the defense process, promoting liver fibrosis formation [42, 56–58]. This evidence concerns the gene NLRP3 and Hepatic fibrosis.