In AD transgenic mice, Aβ treatment induced a high level of caspase-1 and IL-1β in the brain tissue [110,111,112], whereas the inhibition of either NLRP3 or caspase-1 in an AD mouse model increased the clearance of Aβ by microglia, reduced the Aβ deposition, and improved cognitive impairment [112,113]. The gene discussed is CASP1; the disease is Alzheimer disease.