Recently, Heneka et al. demonstrated that the activation of the NLRP3 inflammasome plays a critical role in AD pathogenesis by mediating the chronic inflammatory response, while inhibition of NLRP3 almost completely protected against memory impairment and decreased Aβ deposition in APP/PS1/NLRP3−/− transgenic mice [35]. The gene discussed is APP; the disease is Alzheimer disease.