Indeed, studies using IL-1R1−/− mice in animal models of gut infection with helminth Trichuris muris [20] and experimental stroke [21] found that IL-1β can function in an IL-1R1-independent manner, while IL-1β exacerbates neuronal apoptosis caused by status epilepticus through a mechanism independent of IL-1R1 [22]. The gene discussed is IL1R1; the disease is status epilepticus.