In autoimmune diseases, including multiple sclerosis (MS), their potential is attributed to (1) targeted depletion of B cells, including autoreactive clones, potentially leading to an “immune reset” [114]; (2) elimination of pathogenic plasma cells producing autoantibodies (e.g., in anti-MOG- or anti-AQP4-mediated MS); and (3) penetration into the CNS, where CAR-T cells can target resident B cells and plasma cells inaccessible to monoclonal antibodies [115] (Table 1). Here, MOG is linked to myeloid sarcoma.