In a collagen antibody-induced arthritis (CAIA) model, Clec12a−/− mice experienced more severe inflammation during CAIA due to the over-activation of myeloid cells [23]; while in multiple sclerosis model, Sagar et al. revealed that CLEC12A/CLL-1 participated in the trafficking of DCs across the blood-brain barrier. This evidence concerns the gene CLEC12A and multiple sclerosis.