In addition to the amount of PRAT, functional changes of PRAT including inflammation, and adipokines might help mediate DN; the amelioration of PRAT inflammation through genetic or exogenous inhibition of plasminogen activator inhibitor-1 (PAI-1) expression improved DN in high-fat diet (HFD)-fed mice [13]; an angiotensin II receptor blocker telmisartan inhibited leptin secretion from PRAT to ameliorate DN, accompanied with suppression of proliferative signaling in the kidney [14]. This evidence concerns the gene LEP and liver dysplastic nodule.