To test our hypothesis that combi-ICI-mediated dysregulation of neuro-immune networks sensitizes the CNS to potential autoimmune neuroinflammatory states, we studied the effect of CTLA-4 and PD-1 blockade in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS)-like disease. This evidence concerns the gene CTLA4 and experimental autoimmune encephalomyelitis.