Interestingly, experiments with Prnp knockout mice involving a diverse set of inflammatory processes (Table 1), such as experimental brain ischemia, brain trauma, experimental autoimmune encephalomyelitis (EAE), experimental colitis, and, intracerebral infection with encephalomyocarditis virus variant B (EMCV-B), have revealed that in the absence of PrPC, inflammatory damage is greatly exacerbated; reviewed by Onodera et al. (118). The gene discussed is PRNP; the disease is experimental autoimmune encephalomyelitis.