Finally, the phenotype of plasma norepinephrine steady-state concentration is not solely dependent on rate of norepinephrine biosynthesis or secretion; inter-individual variability in the steady-state concentration of plasma catecholamines can also be determined by removal processes including reuptake (by NET1 or OCT3) or metabolism/degradation (by COMT or MAOA/MAOB); indeed, when plasma norepinephrine is elevated in uremia, one causative factor seems to be diminished plasma clearance of the amine [22]. This evidence concerns the gene MAOA and uremia.