Wen et al. [100] reported that deregulated, continuous high expression of IL-5 in SLE-prone mice may directly or indirectly mediate a skewed signaling of proliferation/differentiation of self-antigen-activated B1 cells, leading to suppression of autoimmune disease, but instead of aberrant expansion of B1 cells, giving rise to B-cell chronic lymphocytic leukaemia (B-CLL). The gene discussed is IL5; the disease is B-cell chronic lymphocytic leukemia.