The impairment of renal clearance in CKD results in the accumulation of toxins, such as p-cresol and indoxyl sulphate, which not only stimulate the expression of intercellular adhesion molecule-1 (ICAM) and monocyte chemotactic protein-1 (MCP-1), but also induce the activation of NADPH oxidase, increasing the production of reactive oxygen species, as well as pose surplus cardiovascular risk in CKD [24,25]. The gene discussed is FMO5; the disease is chronic kidney disease.