CD40/CD40L interaction has been reported to enhance the inflammatory response in multiple sclerosis, and genetic ablation or antibody-mediated inhibition of the CD40/CD40L interaction reduces the severity of experimental autoimmune encephalomyelitis (EAE), a murine model for multiple sclerosis (Gerritse et al., 1996; Grewal et al., 1996; Aarts et al., 2017). This evidence concerns the gene CD40LG and experimental autoimmune encephalomyelitis.