Besides its physiological roles, our [18] and other investigators' recent data [28] indicate that homeostatic proliferation is likely involved in maintaining and/or expanding autoreactive T cells during MS with the result of premature senescence of T cells and narrowing of the T cell repertoire [37] and probably also a factor that contributes to increased secondary autoimmunity following treatment with the depleting anti-CD52 antibody alemtuzumab [28]. Here, CD52 is linked to myeloid sarcoma.