Halle et al. found that fibrillar Aβ can induce the secretion of IL-1β which depends on the presence of NLRP3.352,353 In APP/PS1 mice model, NLRP3 knockout reduced Aβ deposition by enhancing phagocytic clearance capacity and increasing extracellular Aβ degradation by insulin- degrading enzyme (IDE).354 Using the same model, Dempsey et al. found that deletion of NLRP3 or caspase-1 promoted microglia to anti-inflammatory phenotype, with reduced expression of IL-1β and caspase-1.355 These data suggest NLRP3 to be a potential target for AD therapy. The gene discussed is IL1B; the disease is Alzheimer disease.