A plethora of studies have demonstrated the functional role of inflammation in DKD, which can be triggered by the interaction of metabolic defects, secondary injury mediators (like angiotensin II and aldosterone) and pathological consequences of kidney cell injury or dysfunction (such as albuminuria, loss of Klotho production, lipid accumulation and lipotoxicity) (34, 35). The gene discussed is KL; the disease is diabetic kidney disease.