As a conclusion, our results indicate that, although metabolic alterations, mainly leptin resistance in the BWF1 mice, slow-down the progression of autoimmunity, the presence of hyperinsulinemia and the sustained insulin stimulation of organs that remain insulin-sensitive, such as the liver and potentially the kidneys, facilitates the overexpression and activity of the mTOR system and the appearance of the clinical symptoms of SLE. The gene discussed is MTOR; the disease is hyperinsulinism.