Besides that, several factors participate in the pathophysiology of CKD: initiation (proinflammatory cytokines such as TNF-α, IL-6, oxidative stress, and TGF-β), transition (TGF-β, CTGF, and NF-κb), and establishment (TGF-β, activation of myofibroblasts, ECM, and collagen types I, II, and IV) where multiple profibrogenic molecules participate [27, 28]. This evidence concerns the gene TNF and chronic kidney disease.