C1q-deficient mice fed with a high-fat diet accumulated lower levels of complement activation products in their livers and were protected from hepatic insulin resistance (51), while CD55 (decay acceleration factor, DAF)-deficient animals, which lack a key negative complement regulator and have therefore increased complement C3 and C5 activation, were more sensitive to the development of insulin resistance and also showed altered lipid handling and increased adiposity (52). The gene discussed is CD55; the disease is Insulin resistance.