APP/PS1 mice lacking either NLRP3 or caspase 1, which are key components for the maturation and secretion of IL-1β, showed improved spatial memory, synaptic plasticity and decreased Aβ levels (Heneka et al., 2013), suggesting a relevant role of the pro-inflammatory cytokine in the progression of AD pathology. The gene discussed is IL1B; the disease is Alzheimer disease.