Consequently, it was demonstrated that myeloid cells are predominantly responsible for mediating NLRP3 inflammasome activation in the liver, determining infiltration of neutrophils and directly promoting the profibrotic phenotype of HSCs, resulting in fibrosis progression.77 The same research group went on to demonstrate the role of IL-18 in mediating activation of HSCs and liver fibrosis. The gene discussed is NLRP3; the disease is Hepatic fibrosis.