Decreased SOD2 expression has been characterized in various disease states such as SCD,26 pulmonary hypertension,21 and chronic kidney disease.41 Given the evidence that therapeutic upregulation of SOD activity attenuates vascular dysfunction,42,43 we hypothesized that SOD2 expression may be essential in modulating disease pathogenesis in conditions in which the vasculature is a primary target such as SCD. This evidence concerns the gene SOD1 and Schnyder corneal dystrophy.