Significant reductions in sympathetic cardiovascular drive, as assessed by the assay of venous plasma norepinephrine or more directly via the microneurographic technique, have been reported in chronic renal failure patients when treated with central sympatholytic agents such as clonidine and moxonidine, the latter drug being evaluated when administered on top of conventional treatment with pharmacologic compounds acting on the renin–angiotensin system [26–28]. The gene discussed is REN; the disease is chronic kidney disease.