Several mechanisms contribute to ROS and RNS formation in tissues of SCD patients such as (i) increased activity of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and endothelial xanthine oxidase (XO) [8,10], (ii) HbS autoxidation [11], (iii) heme and iron release, (iv) increased asymmetric dimethylarginine (ADMA) [12,13], and (v) uncoupling of nitric oxide synthase (NOS) activity and decreased •NO bioavailability [20]. The gene discussed is XDH; the disease is Schnyder corneal dystrophy.