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. The gene discussed is IL17A; the disease is myeloid sarcoma.