In this study, it was hypothesized that impaired function of AD-associated mutant TOMM40 including (F113L) and (F131L) TOMM40 could cause the accumulation of mitochondrial Aβ and result in mitochondrial malfunction and oxidative stress of microglia, leading to the activation of microglia and the NLRP3 inflammasome, the release of neurotoxic pro-inflammatory cytokines, and the subsequent cell death of hippocampal neurons. The gene discussed is NLRP3; the disease is Alzheimer disease.