Additional studies have examined the impact of defective leptin signaling on a systemic lupus erythematosus prone MRL/Mp-Fas(lpr) mouse model, which spontaneously develops human disease-like lesions, autoantibody production against self-antigens, proliferative glomerulonephritis, and hypocomplementemia (Fujita et al., 2014). This evidence concerns the gene LEP and systemic lupus erythematosus.