Since not only IL-1β, but also endogenous IL-1α and IL-1ra are able to bind to IL-1 receptors, these results suggest that the effect of exogenous IL-1ra on both astrocyte activity and P450c17 expression is mediated in large part by blockade of IL-1β’s action in this neuropathic pain model. The gene discussed is IL1B; the disease is neuropathic pain.