This suggests a dose-related difference, or that perhaps the genetics of people with MS and other potential autoimmunities (7) may also predispose them for generating immune responses that may contribute to generating ADA responses; (f) Lastly, since peripheral B cell niches may not be effectively purged, and CD52 is only weakly expressed by plasmablasts and plasma cells (Figure 1) (51, 52), alemtuzumab may not particularly target antibody-forming cells. This evidence concerns the gene ADA and myeloid sarcoma.