Given the compelling positive link between IDO activity and major depressive symptoms, highlighted by clinical studies examining the depressive side-effects of IFN-α-based immunotherapy (Bonaccorso et al., 2002a), a more favorable therapeutic entry-point for MS might be based on the hypothesis that selected downstream KP metabolites serve to limit autoimmunity by influencing T-cell differentiation toward regulatory phenotypes. This evidence concerns the gene IFNA1 and myeloid sarcoma.