Administration of IL-33 has been shown to modulate the innate immune response by polarising microglia/macrophages towards an anti-inflammatory phenotype and reducing the expression of proinflammatory genes (Il1b, Il6 and Nlrp3) in the cortices of APP/PS1 mice, an experimental model of Alzheimer's disease (Fu et al., 2016). The gene discussed is IL1B; the disease is Alzheimer disease.