Conversely, chronic AD-like inflammation, independent of NLRP3 inflammasome activation, relies on IL-1β and IL-1 receptor 1 (IL-1R1) signaling (11). A recent study reported that an NLRP3 inflammasome inhibitor enhances imiquimod-induced chronic itch through the NLRP3/Caspase-1/IL-1β axis (12). The gene discussed is NLRP3; the disease is Alzheimer disease.