Indeed, in association with their smaller cerebral infarct volume (discussed above), myeloid cell MR-deficient mice also have fewer activated microglia, macrophages and pro-inflammatory mediators (IL-1β and TNFα) in the ischemic core compared to control mice[25], implicating immune cell-expressing MR as important mediators of inflammation in ischemic stroke. The gene discussed is NR3C2; the disease is ischemic stroke.