Whereas the inhibition of B-cell apoptosis, observed in old BIM deficient mice or after the B-cell overexpression of BCL2, causes SLE in predisposed animals [3–5], the dysregulation of this pathway in T cells blocks the development of autoimmune diseases in young BIM deficient mice or in BCL2- or BCLX-TgT mice [10–13]. Here, BCL2L11 is linked to autoimmune disease.