Activation of intrarenal NLRP3 inflammasomes releases IL-1β, IL-18 and other pro-inflammatory cytokines, which is associated with increased renal inflammation, injury, and fibrosis, and reduced renal function, whereas NLRP3 inhibition induces a shift of infiltrating renal macrophages from a pro-inflammatory and profibrotic phenotype to an anti-inflammatory and anti-fibrotic phenotype, and prevents renal injury and fibrosis in CKD animals and human patients [38, 48]. The gene discussed is IL1B; the disease is chronic kidney disease.