In CKD, RAS has been directly linked with enhanced oxidative stress and CKD progression through the up-regulation of pro-oxidative pathways (NF-kB, NADPH oxidase, cyclooxygenase 2, 12-lipooxygenase) by angiotensin II and its binding to angiotensin-1 receptor [159]. This evidence concerns the gene NFKB1 and chronic kidney disease.