Finally, even though a number of other metabolic defects have been reported in liver in CKD [1–3], possibly occurring through the P38 MAP kinase-mediated inflammatory injury that is observed in models of liver injury [4–9], measurements of P38 and JNK MAP kinase activation in the present study detected no statistically significant activation of these kinases in the NxC rats (Fig. 1a, b), nor did measurements of the LFT enzyme ALT detect any abnormality (Fig. 1c). This evidence concerns the gene GPT and chronic kidney disease.