The fact that unmutated and mutated CLL cells derive from self-reactive precursors [61], the suggestion that CLL cells are in active (auto)antigen-driven receptor editing [64], autocrine IL-10 secretion during CD5+ stimulation in leukemic CLL B cells [72, 74], and that most if not all cases of CLL involve the production of polyreactive monoclonal antibodies that react with several types of autoantigens, support the idea that CD5 expression in CLL might be related to the control of autoimmunity. The gene discussed is IL10; the disease is B-cell chronic lymphocytic leukemia.