Given that cDNA-uPA/SCID mice developed additional pathological features in kidney and spleen, using other immunodeficient mice in the C57BL/6 background might be a better approach to develop a humanized model of obesity, insulin resistance and NAFL to enable studies on the effects of hyperinsulinemia, hyperlipidemia and glucotoxicity on human hepatocytes. This evidence concerns the gene PLAU and obesity due to melanocortin 4 receptor deficiency.