When inhibited during status epilepticus (one of possible key initiating events in epileptogenesis), C5ar1 decreases production of tumor necrosis factor alpha (TNFα)10, which along with interleukin 1 beta (IL-1β), are key proinflammatory cytokines known to promote and initiate detrimental processes including microglial activation resulting in neuronal damage, and subsequent hyperexcitability14. The gene discussed is IL1B; the disease is status epilepticus.