A role for TNF deficiency in the induction of autoimmunity in humans is supported by the finding that up to 50% of patients with autoimmune disorders treated with TNF inhibitors develop de novo anti-nuclear antibodies (ANAs), 15% develop antibodies against DNA and/or cardiolipin, and 0.2%–1% develop clinical SLE that often remits upon cessation of treatment (22–24). Here, TNF is linked to hyperinsulinemic hypoglycemia, familial, 4.