Studies on knockout uPA−/− and uPAR−/− mice showed the involvement of uPA/uPAR in the regulation of CNS inflammation: uPA/uPAR deficiency led to more severe manifestation of experimental autoimmune encephalomyelitis with higher levels of microglia activation and exacerbated neuronal injury and death [101]. The gene discussed is PLAU; the disease is experimental autoimmune encephalomyelitis.