The authors demonstrated that C1q limits tissue damage by acting as a “metabolic rheostat” for effector CD8+ T cells that drive autoimmune inflammation through the generation of autoantigen fragments via granzyme B. In contrast to patients with C1q deficiency, only 10%–20% of patients with a C2 deficiency develop lupus (29). The gene discussed is C2; the disease is hyperinsulinemic hypoglycemia, familial, 4.