Sickle cell disease (SCD) is an inherited hemoglobinopathy that results in sickling of deoxygenated red blood cells (RBC) due to a point mutation in the beta-globin gene.1 In SCD, there is an increase in oxidative stress due to augmented reactive oxygen species (ROS) production from enzymatic sources such as xanthine oxidase2 and non-enzymatic sources including Fenton chemistry.3 Paired with this increase in ROS production is a compromised antioxidant system. This evidence concerns the gene HBB and Schnyder corneal dystrophy.