Thus, mice and humans with mutations in fas/fasL, transgenic (Tg) mice overexpressing human BCL2 (hBCL2) in B lymphocytes or mice with a targeted disruption of BIM, a pro-apoptotic BCL2 relative, develop an autoimmune syndrome resembling systemic lupus erythematosus (SLE) in association or not with lymphoproliferation [1–5]. Here, BCL2L11 is linked to systemic lupus erythematosus.