Recent evidence has linked cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed death-1 (PD-1), T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibition motif domains (TIGIT), and T cell immunoglobulin- and mucin domain-containing molecule 3 (TIM-3) as important immune regulatory pathways in the resolution of EAE, showing a strong genetic or functional correlation in MS (reviewed in [4]). This evidence concerns the gene HAVCR2 and myeloid sarcoma.