Thus, reduced IFN signaling in Cstb-/- mice might elevate inflammasome activation and induce the activation of the pro-inflammatory cytokines IL1β and IL18, which have been shown at high levels in the serum of LPS-injected Cstb-/- mice [11] and have been linked to the pathogenesis of several neurodegenerative diseases, such as Alzheimer’s disease and multiple sclerosis [56]. The gene discussed is IL18; the disease is early-onset autosomal dominant Alzheimer disease.