Zhao et al. showed that Klotho overexpression inhibited PYD domain-containing protein 3 (NLRP3) inflammasome activation and promoted Aβ clearance through an increase in M2 type microglia and the regulation of Aβ transporters in amyloid precursor protein/presenilin 1 (APP/PS1) mice, with effectively relieved neuroinflammation and Aβ burden and ameliorated Alzheimer’s Disease (AD)-like phenotypes (36). The gene discussed is APP; the disease is Alzheimer disease.