Overactivation of the NLRP3 inflammasomes in microglia transforms them into a proinflammatory phenotype, resulting in reduced phagocytosis of Aβ‐42 by microglia, which can lead to enhanced Aβ deposition and progression of AD pathogenesis (Lučiūnaitė et al., 2020). The gene discussed is NLRP3; the disease is Alzheimer disease.