20, 21, 22, 23 In addition, NLRP3 activation in microglia is reported to contribute to the progression of AD-like pathology in APP/PS1 transgenic mice, and NLRP3 knock out (KO) mice are reported to have decreased disease burden.24 Although oAβ is postulated to activate inflammasomes,25 how oAβ induces NLRP3 activation to process pro-IL-1β to the mature form remains unknown. The gene discussed is NLRP3; the disease is Alzheimer disease.