Non-autoimmune mice rendered genetically deficient in estrogen or its receptors develop expanded B lymphoid and myeloid cell pools (Shim et al. 2003), plasmacytosis (Shim et al. 2004a), and autoimmunity (Shim et al. 2004a; Shim et al. 2004b), including lupus-like immune complex glomerulonephritis (Shim et al. 2004a), whereas induction of ER-alpha deficiency in (NZBxNZW)F1 lupus mice leads to amelioration of autoimmune disease (Bynote et al. 2008). This evidence concerns the gene ESR1 and hyperinsulinemic hypoglycemia, familial, 4.