Polymorphisms in the genes involved in pathways such as those associated with inflammatory reactions (e.g., tumor necrosis factor (TNF)-α and interleukin (IL)-4), fibrosis (e.g., TGFB1), phase-II metabolism (e.g., GSTP1 and GSTO1), CKD worsening (e.g., UMOD) and the renin–angiotensin–aldosterone system (RAAS) (e.g., AGT and RENBP) have been suggested to affect the progression rate of patients with CKD [13]. This evidence concerns the gene TNF and chronic kidney disease.