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]. This evidence concerns the gene PLAUR and experimental autoimmune encephalomyelitis.