The idea of DMF-mediated diversion of Tc17 profile towards a “CTL-like” genetic signature is based on the comparison of memory CD8+ T cells from untreated versus treated MS patients with IL-17+CD8+ versus IL-17−CD8+ T cell from healthy individuals, which profiles were recently published42, as well as with our datasets on gene expression in mouse effector Tc17. This evidence concerns the gene CD8A and myeloid sarcoma.