Future in-vitro studies which directly measure aortic NOS bioactivity and levels of both eNOS and the phosphorylation of serine 1177 of eNOS, reflecting the activated form of the protein (Boo et al., 2002) will greatly inform our overall understanding of the mechanisms driving changes in NO bioavailability and NOS sensitivity in large vessels associated with kidney disease. The gene discussed is NOS3; the disease is kidney disorder.