The mechanism by which complement is activated by MBP—and other self-antigens such as thyroglobulin (TG) [47]–remains to be elucidated, but the presence of MBP-reactive antibodies in normal human serum and in serum from MS patients [48,49] suggests that immune complexes containing MBP activate complement through the classical pathway leading to tagging of MBP with fragments of complement component 3. The gene discussed is TG; the disease is myeloid sarcoma.