More specifically, experimental models indicate that p-cresyl sulfate, a uremic toxin that accumulates with CKD progression, enhances the activity of Nox4-, p22phox-NADPH, and ROS production in renal tubular cells, which in turn induces the expression of inflammatory cytokines and profibrotic factors, leading finally to reduced cell viability [80]. This evidence concerns the gene NOX4 and chronic kidney disease.