Several years after the discovery of CD6 as a risk locus for MS, Li et al. demonstrated that CD6-deficient mice (CD6−/−) display decreased pathogenic Th1 and Th17 cells, reduced T-cell infiltration in the spinal cord, and diminished disease severity in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS [58]. The gene discussed is CD6; the disease is experimental autoimmune encephalomyelitis.