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 hyperinsulinism.